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Biomedical subjects

H Hayashi

Publications and source records attributed to H Hayashi.

At least 505 records · Page 28Linked to original sources
PubMed1998

[Clinical usefulness of "optimal threshold setting plan" for reconstruction of three-dimensional CT imaging: preliminary clinical study on hepatic tumors and hepatic parenchymal disease].

Clinical application of three-dimensional CT (3D-CT) angiography using the volumetric acquisition capabilities inherent in spiral CT has provided 3D-CT images of vascular structures as well as visceral organs. However, the standard method for deciding the threshold, which is an important process for defining regions of interest, has not yet been established. The setting of an inappropriate threshold may result in reconstruction of a 3D-CT image, leading to misdiagnosis. To simplify the determination of the optimal threshold in a way consistent with the purpose of reconstructing a 3D-CT image, we developed an Optimal Threshold Setting Plan (OPT Plan). With this method, an optimal 3D-CT image could be selected from among those multiple 3D-CT images that were reconstructed on the basis of the multiple thresholds input in advance by referring to attenuation values in both the hepatic lesion and its background on two-dimensional CT images. Clinical usefulness of the OPT Plan for the reconstruction of 3D-CT images was evaluated in 10 patients with hepatic tumors and hepatic parenchymal disease. We obtained 13 3D-CT images (on average) with threshold changes every 5 Hounsfield units, with a mean reconstruction time of 2 minutes 49 seconds, and easily selected an adequate 3D-CT image. Based upon this preliminary experience, the OPT Plan may resolve the difficulty encountered in the setting of thresholds for achieving 3D-CT images, and is considered to be useful for three-dimensional qualitative evaluation of hepatic lesions and hepatic parenchymal disease.

Adult↗
PubMed1998

[Chronic progressive radiation myelopathy after bone marrow transplantation].

Two patients after bone marrow transplantation (BMT) developed chronic progressive radiation myelopathy (CPRM). The factors contributing to development of CPRM at the low dose, which radiation doses given for enlarged regional lymph nodes prior to BMT ordinarily would be too low to induce CPRM, were discussed, and clinicoradiologic correlations in CPRM from onset through the stabilized state examined. The clinicoradiologic findings of two patients, who are a 26-year-old man with malignant lymphoma (autologous BMT) performed radiotherapy totaling 20 Gy for enlarged regional lymph nodes before BMT, and a 40-year old woman with chronic myeloid leukemia (allogenic BMT) done 18.9 Gy, were examined. The involved spinal cord segments were irradiated for lymph node enlargement prior to BMT, and all the clinicoradiologic findings were consistent with CPRM. We considered possible synergistic toxicity with high-dose busulfan accompanying BMT. Unlike the second case, the first patient had continued severe progression of CPRM, possibly because a higher dose of additional radiotherapy (30 Gy) was given for presumed spinal cord tumor involvement in that case than in the other (< 20 Gy). These cases demonstrate that BMT protocols carry a risk of potentiating the spinal cord toxicity of low-dose radiotherapy.

Adult↗
PubMed1998

[Anaphylaxis in a myelodysplastic syndrome patient during platelet transfusion with a leukocyte-reduction filter].

A 77-year-old woman with myelodysplastic syndrome required platelet transfusion. However, she complained of facial flushing and dyspnea immediately after the initiation of an infusion of platelet concentrations (PC) utilizing a Pall PL-PXL8H filter with a negatively charged surface. The same symptoms recurred following a transfusion of washed PC with saline. However, an infusion utilizing a Sepacell PLX5A-W with a positively charged surface caused no problems. Furthermore, the patient demonstrated the same adverse reaction after administration of prostaglandin F2 alpha. This case suggested that special caution is warranted when patients who have an allergic history receive PC infusions through leukocyte-reduction filters with negatively charged surfaces.

Aged↗
PubMed1998

[Outcomes of stroke survivors in Yamagata Prefecture].

PURPOSE: To clarify the long-term outcomes of Stroke survivors registered for the first onset of Stroke in Yamagata Prefecture and to find out problems in community-based-rehabilitation (CBR). SUBJECTS AND METHODS: The present study was performed using stroke survivors as of September 1, 1991 as subjects from residents registered for the onset of Stroke in 1985 and 1989. The subjects were composed of 1,013 residents registered in 1989 (2 years after onset) and 626 registered in 1985 (6 years after onset). RESULTS: The percent of functionally-independent Stroke survivors at 2 and 6 years (indicated in parentheses) after onset is shown by ADL items as follows: 82% (81%) for urination, 78% (78%) for eating, 78% (78%) for walking, 76% (78%) for dressing, and 66% (64%) for bathing. The lowest percent was seen in Bathing. Percentage of cases maintaining the ability to have functionally-independent ADL for all items examined (expressed as persons independent for personal care) were 62% (60%). Of the the cases 91% (91%) resided at home (their own houses or relatives' houses). With regard to overall locomotion, an item used to evaluation the range of going out doors, 45% (44%) could go out alone to visit neighbors or use public transportation. Among persons independent for personal care, 99% (98%) were living at homo, 70% (69%) used public transportation, 23% (23%) went out alone to visit neighbors and 7% (8%) did not go out. CONCLUSION: The results of the present research indicate a great in CBR for that bothpsychological and social health approaches in cooperation with public health centers, medical centers, and welfare agencies not only for persons with decreased ADL, but also for those maintaining high activity potential.

Activities of Daily Living↗
PubMed1997

Prominent sensory and autonomic disturbances in familial amyotrophic lateral sclerosis with a Gly93Ser mutation in the SOD1 gene.

A missense mutation (Gly93-->Ser) was identified in exon 4 of the Cu/Zn superoxide dismutase (SOD1) gene of a 48-year-old Japanese man with familial amyotrophic lateral sclerosis (FALS). The SOD1 activities in the fibroblasts and in a lysate of erythrocytes of the patient did not differ from those of healthy controls. The clinical characteristics of the patient were fairly slow progression of the illness, prominent sensory impairment, urinary disturbance and blood pressure fluctuation due to sympathetic hyperactivity. The severe sensory and autonomic disturbances, association of which with FALS has not been previously reported, may represent specific clinical features associated with the Gly93Ser mutation or may indicate the variability of clinical findings even in patients with the same mutation.

Amyotrophic Lateral Sclerosis↗
PubMed1997

Metabolic methylation is a possible genotoxicity-enhancing process of inorganic arsenics.

To elucidate if the metabolic methylation participates in the induction of inorganic arsenic-responsible genetic damage, arsenite (ARS) and its methylated metabolites, methanearsonic acid (MMAA) and dimethylarsinic acid (DMAA), were comparatively assayed for the induction of DNA damage by determining DNA repair synthesis using polymerization inhibitors such as aphidicolin (aph) and hydroxyurea (HU). When human alveolar epithelial type II (L-132) cells in culture were exposed to either one of these three arsenic compounds, DNA single-strand breaks resulting from the inhibition of repair polymerization were remarkably produced by exposure to DMAA at 5 to 100 microM, while not by that to ARS and MMAA even at 100 microM. Furthermore, a bromodeoxyuridine (BrdrU)-photolysis assay indicated that the induction of DNA repair synthesis was observed only in the case of exposure to DMAA. When L-132 cells were exposed to 100 microM MMAA in the presence of 10 mM S-adenosyl-L-methionine (SAM), which is a well-known methyl-group donor in metabolic methylation of arsenics, DNA repair synthesis was induced along with an increase in the amount of dimethylarsenic in the cells. These results indicate that metabolic methylation of inorganic arsenics to dimethylarsenics is predominantly involved in the induction of DNA damage.

Arsenic Poisoning↗
PubMed1997

Hyperinsulinemia but no diabetes in transgenic mice homozygously expressing the tyrosine kinase-deficient human insulin receptor.

We generated transgenic mice homozygous for the tyrosine kinase-deficient human insulin receptor (hIRK1030M(+/+)) under control of the insulin receptor promoter. Similar growth patterns and results of glucose tolerance tests were observed among normal, heterozygous, and homozygous mice. Insulin tolerance test indicated no significant difference in the hypoglycemic response to insulin among the three genotypes. However, the serum insulin levels of the homozygous mice before and after glucose loading (201.42 +/- 58.15 pg/ml to 578.57 +/- 49.03 pg/ml) were significantly higher than in the control mice (100.92 +/- 19.55 pg/ml to 356.36 +/- 55.08 pg/ml; p < 0.01 and p < 0.01, respectively) and heterozygous mice (74.46 +/- 18.55 pg/ml to 352.33 +/- 52.43 pg/ml; p < 0.005 and p < 0.01, respectively). Immunohistological evidence of pancreatic islets showed no significant difference among the three genotypes. Taken together, these results suggest that the tyrosine kinase-deficient insulin receptor causes hyperinsulinemia but not diabetes in these homozygous transgenic mice.

Animals↗
PubMed1997

Transient-state kinetics of the reaction of aspartate aminotransferase with aspartate at low pH reveals dual routes in the enzyme-substrate association process.

In aspartate aminotransferase, the coenzyme pyridoxal 5'-phosphate forms a Schiff base with the epsilon-amino group of Lys258. The pH dependency of the steady-state kinetics of the overall reaction had indirectly suggested that the Schiff-base-unprotonated form of the enzyme (EL) is the active species that binds the monoanionic form of aspartate (SH+), the predominant species of the substrate in solution. In order to obtain direct information on the association process, we carried out transient-phase kinetics of the first half-reaction of the enzyme with aspartate at various pH. The disappearance of EL (lambdamax = 358 nm) was fast and independent of pH, but the disappearance of ELH+ (Schiff-base-protonated form, lambdamax = 430 nm) was slow and dependent on pH. At pH values below 6.8 and low concentrations of aspartate, the results could be interpreted to indicate that EL reacts rapidly with SH+ to form the pyridoxamine 5'-phosphate form of the enzyme (EM), and the reaction of ELH+ proceeds via the route ELH+ right arrow over left arrow EL right arrow over left arrow EM, where the first step was found to be rate limiting from the pH jump/drop study of the enzyme. At higher pH values, the rate of disappearance of ELH+ became larger than expected from the above scheme. This deviation became apparent with increasing pH, and could be excellently explained if we consider that it is due to the reaction of ELH+ with the dianionic form of aspartate (S). Thus, the formation of the Michaelis complex of aspartate aminotransferase and aspartate can proceed via two routes; route A is the association of EL with SH+ to form EL.SH+, which converts intramolecularly to ELH+.S, and route B is the association of ELH+ with S to form ELH+.S directly. ELH+.S is the prerequisite structure for further processing of the substrate by the enzyme. The reactions of EM and oxo acids yielded almost exclusively EL and SH+, and therefore route B does not seem to play an essential role in the overall reactions of the enzyme. Route B, however, may be important in the reaction mechanisms of other pyridoxal 5'-phosphate enzymes which have only the ELH+ form.

Aspartate Aminotransferases↗
PubMed1997

TbetaRI phosphorylation of Smad2 on Ser465 and Ser467 is required for Smad2-Smad4 complex formation and signaling.

Mothers against Dpp-related or Smad proteins are essential components of serine/threonine kinase receptor signaling pathways that are regulated by phosphorylation. Recently, it was demonstrated that Smad2 interacts transiently with and is a direct substrate of the transforming growth factor-beta (TGF-beta) type I receptor, TbetaRI. Phosphorylation sites on Smad2 were localized to a carboxyl-terminal fragment containing three serine residues at positions 464, 465, and 467. In this report, we show that TbetaRI specifically phosphorylates Smad2 on serines 465 and 467. Serine 464 is not a site of phosphorylation, but is important for efficient phosphorylation of Smad2. Phosphorylation at both sites is required to mediate association of Smad2 with Smad4 in mammalian cells, while in yeast, Smad2 interacts directly with Smad4 and does not require phosphorylation. Mutation of either serine residue 465 or 467 prevents dissociation of Smad2 from activated TbetaRI and blocks TGF-beta-dependent signaling and Smad2 transcriptional activity. These results indicate that receptor-dependent phosphorylation of Smad2 on serines 465 and 467 is required in mammalian cells to permit association with Smad4 and to propagate TGF-beta signals.

Activin Receptors, Type I↗
PubMed1997

Body-surface distribution of changes in activation-recovery intervals before and after catheter ablation in patients with Wolff-Parkinson-White syndrome: clinical evidence for ventricular 'electrical remodeling' with prolongation of action-potential duration over a preexcited area.

BACKGROUND: T-wave abnormalities after catheter ablation in patients with manifest Wolff-Parkinson-White (WPW) syndrome have been attributed to a continuation of repolarization abnormalities induced by preexcitation (cardiac memory). METHODS AND RESULTS: To clarify changes in repolarization properties, we analyzed the activation-recovery interval (ARI) obtained from body-surface maps and the relationship between the activation time (AT) and ARI in 30 patients with WPW syndrome (group A, 18 patients with manifest left-sided accessory pathway; group B, 7 patients with manifest right-sided accessory pathway; and group C, 5 patients with concealed left-sided accessory pathway) before, 1 day after, and 1 week after ablation. The ARI significantly decreased 1 week after ablation compared with before and 1 day after ablation over the preexcited area in groups A and B. Correlation coefficients between the AT and ARI showed a significantly (P<.01) stronger inverse relationship before (r=-.58) and 1 week after (r=-.64) ablation than 1 day after ablation (r=-.46) in groups A and B. In group C, the ARI and correlation coefficients between the AT and ARI showed no significant changes. CONCLUSIONS: These findings suggest a prolongation of the action-potential duration over the preexcited area before and just after ablation as ventricular "electrical remodeling," a decrease in the inverse relationship between the AT and action-potential duration 1 day after ablation, and a gradual recovery of the action-potential duration over the preexcited area and inverse relationship 1 week after ablation.

Action Potentials↗
PubMed1997

Circadian rhythms of cardiovascular functions are modulated by the baroreflex and the autonomic nervous system in the rat.

BACKGROUND: We assessed the hypothesis that the baroreflex and the autonomic nervous system are important in the control of the circadian rhythms of cardiovascular functions. METHODS AND RESULTS: We continuously measured blood pressure (BP), heart rate (HR), and locomotor activity in sinoaortic denervated (SAD), sympathectomized, and atropine-injected rats by use of a radiotelemetry system. The circadian rhythm of mean blood pressure (MBP) was selectively disrupted in SAD rats under 12-hour light-dark (LD12:12) cycles as a result of an increase in MBP during the light period and disappeared under constant darkness (DD). The locomotor activity and HR were not remarkably affected by SAD. The circadian rhythm of MBP was suppressed in sympathectomized rats by a decrease in the MBP during the dark period, and the abrupt changes in MBP when the lighting was altered were not seen under LD. Under DD, an MBP rhythm similar to that observed under LD was obtained. Sympathectomized rats also showed lower HR levels during the dark period than intact rats under LD cycles. In atropine-injected rats, the MBP and HR increased, especially during the light period, resulting in a reduction of light-dark differences in MBP and HR. The locomotor activity showed an apparent 24-hour variation in the sympathectomized and atropine-injected rats. CONCLUSIONS: The disruption of the baroreflex selectively eliminates the circadian rhythm of BP, and the circadian rhythms of BP and HR are modulated by the autonomic nervous system in rats. The circadian rhythms of BP and HR are regulated by different mechanisms involving the autonomic nervous system.

Animals↗
PubMed1997

Reevaluating the effects of tyrosine iodination of recombinant hirudin on its thrombin inhibition kinetics.

To reevaluate the effects of iodination of hirudin on its thrombin-inhibiting activity, we iodinated a recombinant hirudin analog, CX-397, by a chloramine-T method and isolated the eight kinds of iodinated derivatives by reverse-phase HPLC. Their structure were different combinations of non-, mono-, or di-iodinated residues at Tyr-3 and Tyr-64. Their ability to inhibit alpha-thrombin were determined and compared with each other. Iodination at Tyr-64 slightly increased the association rate constant (Kon) 1.26- to 1.79-fold; this may be explained by the increase in the negative charge at C-terminal region of CX-397 caused by the electrophilic ortho substitution of Tyr-64 with iodine. On the contrary, iodination at Tyr-3 caused dual effects on the interaction between CX-397 and alpha-thrombin; namely, mono-iodination at Tyr-3 caused a small decrease in Koff (1.29- to 1.63-fold) than non-iodinated ones, whilst di-iodination at Tyr-3 brought about 3.04- to 3.88-fold increase in Koff. Since the N-terminal region of hirudin has been reported to bind with thrombin by hydrophobic interaction, the destabilizing effect of di-iodination at Tyr-3 can be explained by the increase in its polar nature, whereas the opposite effect of mono-iodination can not. These results indicate that it is not appropriate to use a mixture of variably radioiodinated hirudins as a radiotracer. We also provide a simple method to obtain well characterized radioiodinated hirudins.

Amino Acid Sequence↗
PubMed1997

OCAM: A new member of the neural cell adhesion molecule family related to zone-to-zone projection of olfactory and vomeronasal axons.

Zone-to-zone projection of olfactory and vomeronasal sensory axons underlies the topographic and functional mapping of chemoreceptor expression zones of the sensory epithelia onto zonally arranged glomeruli in the main and accessory olfactory bulbs. Here we identified OCAM (R4B12 antigen), an axonal surface glycoprotein expressed by subsets of both olfactory and vomeronasal axons in a zone-specific manner. OCAM is a novel homophilic adhesion molecule belonging to the immunoglobulin superfamily with striking structural homology to neural cell adhesion molecule. In both the main and accessory olfactory systems, OCAM mRNA is expressed by sensory neurons in restricted chemoreceptor expression zones, and OCAM protein-expressing axons project to the glomeruli in the corresponding zones of the main and accessory bulbs. OCAM protein is expressed on subsets of growing sensory axons in explant cultures even in the absence of the target bulb. These results demonstrate a precisely coordinated zonal expression of chemoreceptors and OCAM and suggest that OCAM may play important roles in selective fasciculation and zone-to-zone projection of the primary olfactory axons.

Amino Acid Sequence↗
PubMed1997

Roles of inhibitors of myosin light chain kinase and tyrosine kinase on cation influx in agonist-stimulated endothelial cells.

Agonist-stimulated Ca2+ influx is critically important to mediate the function of endothelial cells. It has been suggested that release of Ca2+ from internal stores activates Ca2+ influx across the plasma membrane. In the present study, we investigated the effects of ML-9, a myosin light-chain kinase (MLCK) inhibitor, and genistein, a tyrosine kinase inhibitor, on the agonist stimulated Ca2+ response in porcine aortic endothelial cells loaded with a Ca2+-sensitive dye, fura-2. ML-9 almost completely abolished Ca2+ influx, whereas genistein only partially attenuated Ca2+ entry. Both of them did not affect the mobilization of Ca2+ from internal stores. In contrast, genistein was more potent in the inhibition of Mn2+ influx than ML-9. These findings indicate the different selectivity for Ca2+ and Mn2+ in the cation entry pathway in agonist-stimulated endothelial cells.

Animals↗
PubMed1997

The MAD-related protein Smad7 associates with the TGFbeta receptor and functions as an antagonist of TGFbeta signaling.

TGFbeta signaling is initiated when the type I receptor phosphorylates the MAD-related protein, Smad2, on C-terminal serine residues. This leads to Smad2 association with Smad4, translocation to the nucleus, and regulation of transcriptional responses. Here we demonstrate that Smad7 is an inhibitor of TGFbeta signaling. Smad7 prevents TGFbeta-dependent formation of Smad2/Smad4 complexes and inhibits the nuclear accumulation of Smad2. Smad7 interacts stably with the activated TGFbeta type I receptor, thereby blocking the association, phosphorylation, and activation of Smad2. Furthermore, mutations in Smad7 that interfere with receptor binding disrupt its inhibitory activity. These studies thus define a novel function for MAD-related proteins as intracellular antagonists of the type I kinase domain of TGFbeta family receptors.

Amino Acid Sequence↗
PubMed1997

Analysis of the Rb gene and cyclin-dependent kinase 4 inhibitor genes (p16INK4 and p15INK4B) in human ovarian carcinoma cell lines.

In the present study, we analyzed human ovarian carcinoma cell lines for abnormalities in the tumor suppressor gene Rb (retinoblastoma) and in cyclin-dependent kinase 4 (CDK4) inhibitor genes (p16INK4 and p15INK4B) using molecular biology techniques. For the Rb gene, in all six cell lines (PA-1, Caov-3 and -4, OVCAR-3, SK-OV-3, and Kuramochi), Rb gene abnormality was not detected using Southern blotting. In the Caov-3 cell line transcripts were not detectable by either Northern blot or polymerase chain reaction. Sequence analysis of the entire coding region of the Rb gene revealed point mutations (AAC to GAC) resulting in codon 123 (Asn to Asp) changes in the Caov-4 cell line. In the PA-1 cell line both wild-type Rb and mutant-type Rb (codon 798: CGG to TGG) were expressed, and in the OVCAR-3 cell line both wild-type Rb and mutant-type Rb (codon 704: ATG to GTG) were expressed. In four of six human ovarian carcinoma cell lines Rb gene abnormality was detected. For the p16INK4 and p15INK4B genes, only the SK-OV-3 cell line had abnormalities. There was a gene rearrangement or minor deletion of the p16INK4 gene in the SK-OV-3 cell line, while the p15INK4B gene was deleted in this cell line. In the SK-OV-3 cell line no mRNAs of p16INK4 and p15INK4B were expressed. At the point of Rb gene inactivation, we can explain five cell lines of six: four cell lines had abnormalities in the Rb gene itself, which is another mechanism by which the Rb gene is inactivated, while one cell line (SK-OV-3) had abnormalities in CDK4 inhibitor genes, another of the inactivation mechanisms of the Rb gene. These data suggest that abnormalities of Rb and CDK4 inhibitor genes (p16INK4, p15INK4B) may be involved in human ovarian carcinogenesis.

Carcinoma↗