Search PubMed⌕ Search

Biomedical subjects

H Nishio

Publications and source records attributed to H Nishio.

At least 109 records · Page 6Linked to original sources
PubMed1998

[Optimal scan parameters of MRCP using HASTE].

For improving the image of fine structures on MRCP, optimal scan parameters were assessed by water-filled phantom using HASTE sequence. Spatial resolution and Contrast-to-Noise Ratio (CNR) were measured at various FOVs and slice thicknesses with a body array coil. High spatial resolution was provided at less than 25 cm in FOV, and narrow phantom under 1 mm in diameter was obscured at more than 30 cm in FOV. Highest CNR was provided at 3 mm slice thickness on a 1.5 T unit, and at 4 mm slice thickness on a 1.0 T unit. Narrow phantom under 1 mm in diameter was depicted clearly on a 1.5 T unit, but irregularly on a 1.0 T unit. Taking required spatial resolution and CNR into consideration, we should determine optimal FOV and slice thickness for the assessment of anatomic details on MRCP.

Biliary Tract↗
PubMed1998

[MR cholangiopancreatography using respiratory triggered half-Fourier RARE technique].

We evaluate the usefulness of MRCP using respiratory triggered HASTE technique in 68 patients. Eleven subsequent slices were obtained for MRCP. To determine the optimal trigger rate, MRCP with various trigger rates were compared in 25 patients. Respiratory triggered MRCP and breath hold MRCP were compared in 68 patients. Respiratory triggered MRCP was also performed in 3 infants. The optimal trigger rate was 10%. In 17 patients who could not stop their breath for 10 seconds, respiratory triggered MRCP were better than breath hold MRCP in 14 (82%) for the source images and in 17 (100%) for the MIP images. Respiratory triggered MRCP could depict cystic duct and main pancreatic duct even in 14 month infant. MRCP with high spatial resolution could be obtained with respiratory triggered HASTE technique in critically ill, or non-cooperative patients.

Adult↗
PubMed1997

Evidence for myosin-binding phosphatase in heart myofibrils.

Protein phosphatase was partially purified from myofibrils of bovine heart by sequential column chromatographies. The purified protein phosphatase was immunologically identified as a delta isoform of PP1 (PP1delta). The myosin-binding subunit (MBS) of myosin-binding phosphatase (MBP) in smooth muscle was co-purified with PP1delta at each step of the sequential column chromatographies. The immunoprecipitation experiment using the polyclonal antibody to MBS showed that PP1delta associates with MBS in the purified phosphatase. In addition, the myosin-binding assay showed that the purified phosphatase has the characteristics of binding to cardiac myosin. These data strongly suggest that MBP, the holoenzyme composed of PP1delta and MBS, is expressed in heart myofibrils.

Animals↗
PubMed1997

Expression and function of murine receptor tyrosine kinases, TIE and TEK, in hematopoietic stem cells.

Two highly related receptor tyrosine kinases, TIE and TEK, comprise a family of endothelial cell-specific kinase. We established monoclonal antibodies against them and performed detailed analyses on their expression and function in murine hematopoietic stem cells (HSCs). TIE and TEK were expressed on 23.7% and 33.3% of lineage marker-negative, c-Kit+ and Sca-1+ (Lin- c-Kit+ Sca-1+) HSCs that contain the majority of day-12 colony-forming units-spleen (CFU-S) and long-term reconstituting cells, but not committed progenitor cells. Lin- c-Kit+ Sca-1+ cells were further divided by the expression of TIE and TEK. TIE+ and TEK+ HSCs as well as each negative counterpart contained high proliferative potential colony-forming cells and differentiated into lymphoid and myeloid progenies both in vitro and in vivo. However, day-12 CFU-S were enriched in TIE+ and TEK+ HSCs. Our findings define TIE and TEK as novel stem cell marker antigens that segregate day-12 CFU-S, and provide evidence of novel signaling pathways that are involved in the functional regulation of HSCs at a specific stage of differentiation, particularly of day-12 CFU-S.

Animals↗
PubMed1997

Inhibitory effect of ethanol on the 5-HT3 receptor-mediated tachycardia in isolated guinea-pig atrium.

The influence of ethanol on 5-hydroxytryptamine (5-HT)-induced tachycardia mediated by 5-HT3 receptor activation in the isolated guinea-pig atrium was studied. Ethanol at 200 mM significantly inhibited 5-HT - but not isoproterenol- or histamine-induced tachycardia in the isolated guinea-pig atrium. The same inhibitory effect was observed in response to 2-propanol and chloral hydrate application. Both 2-propanol at 100 mM and chloral hydrate at 1 mM exhibited inhibitory effects on 5-HT -induced tachycardia as potent as those of ethanol at 200 mM. These alcohols did not inhibit the tachycardia induced by isoproterenol or histamine. The inhibitory effects of the alcohols seemed to be specific for 5-HT and to increase according to their lipophilicity. Our results suggest that the inhibitory effects of ethanol on 5-HT3 receptor-mediated tachycardia are related to the direct effect of ethanol on 5-HT3 receptors in the atrium.

1-Propanol↗
PubMed1997

Hunter disease in a girl caused by R468Q mutation in the iduronate-2-sulfatase gene and skewed inactivation of the X chromosome carrying the normal allele.

Hunter disease is an X-linked recessive mucopolysaccharide storage disorder caused by iduronate-2-sulfatase deficiency and is rare in females. We describe here findings in a girl with Hunter disease of the severe type. She had a normal karyotype but a marked deficiency of iduronate-2-sulfatase activity in lymphocytes and cultured fibroblasts. In a sequence analysis of the iduronate-2-sulfatase gene, evidence was obtained for the R468Q (G1403 to A) mutation, a common one in Hunter disease. RT-PCR showed her cDNA to represent only the R468Q allele, although at the genomic level she was a heterozygote with one normal allele. Her brother had the R468Q mutation, and their mother was a carrier of this mutation. The fusion products of CHO (TG(R),Neo(R)) with patient's fibroblasts cultured in HAT/G418 selective medium, carried only the maternal allele. However, in genomic DNA from the patient's fibroblasts, only the paternal allele of the androgen receptor gene, a gene subjected to differential methylation of the inactive X-chromosome, was methylated. These findings strongly suggest that the severe form of Hunter disease in this girl was the result of selective expression of the maternal allele carrying the missense mutation R468Q, which in turn resulted from skewed X inactivation of the paternal nonmutant X chromosome.

Alleles↗
PubMed1997

5-Hydroxytryptamine-facilitated release of substance P from rat spinal cord slices is mediated by nitric oxide and cyclic GMP.

The role of nitric oxide (NO) in the control of 5-hydroxytryptamine (5-HT)-induced release of substance P was investigated in rat spinal cord in vitro. 5-HT facilitated the 60 mM K(+)-evoked release of substance P-like immunoreactive materials (SPLI) from the superfused rat dorsal spinal cord slices without affecting spontaneous SPLI release. The facilitatory effect of 5-HT was significantly inhibited by ICS 205-930 or granisetron (potent and specific 5-HT3 receptor antagonists), by NG-monomethyl-L-arginine (NMMA, a NO synthase inhibitor), and by methylene blue or 1H-[1,2,4] oxadiazolo [4,3-a] quinoxaline-1-one (MB or ODQ, respectively; both are inhibitors of soluble guanylyl cyclase) and was mimicked by 2-methylserotonin (2-m-5-HT, a selective 5-HT3 receptor agonist), L-arginine (a precursor of NO), or 8-bromo-cyclic GMP. NMMA, MB, or ODQ inhibited the 2-m-5-HT-induced increase of cyclic GMP levels in the rat dorsal spinal cord slices. These data suggest that the facilitatory effect of 5-HT on the release of SPLI is mediated by the 5-HT3 receptor and that the intracellular signaling is mediated via NO by an increase in cyclic GMP production.

Animals↗
PubMed1997

Early cardiac failure in a child with Becker muscular dystrophy is due to an abnormally low amount of dystrophin transcript lacking exon 13.

Two Japanese brothers with Becker muscular dystrophy were shown by polymerase chain reaction (PCR) and cDNA sequence analysis to produce a dystrophin gene transcript lacking a single exon: that is, number 13. Despite having the same deletion mutation, the brothers showed clearly different clinical phenotypes: the younger brother developed cardiac failure at the age of nine, while the elder brother was asymptomatic. As alternative splicing was not responsible for this clinical difference, the amount of dystrophin transcript was examined by using reverse transcription semi-nested and parallel PCR. The results showed that the amount of the dystrophin transcript in the younger brother was 20% of that of the elder brother. This finding suggested that lesser amount of dystrophin transcript in the younger brother was responsible for the early onset of cardiac failure. This would represent a novel molecular mechanism for dystrophinopathy.

Cardiac Output, Low↗
PubMed1997

Decreased expression of full-length mRNA for cBCD541 does not correlate with spinal muscular atrophy phenotype severity.

Spinal muscular atrophy (SMA) is characterized by degeneration of spinal cord anterior horn cells and muscular atrophy and has three phenotypes based on clinical severity and age of onset. One of the responsible genes for SMA is the survival motor neuron (SMN) gene, which is homozygously absent or interrupted in more than 90% of SMA patients. The cBCD541 (BCD) gene is a highly homologous copy of the SMN gene, which has a single synonymous transition in the coding region and may compensate for the loss of the SMN gene. To evaluate the effects of the BCD gene expression on the phenotypes of SMA, we examined lymphocyte mRNA from 9 SMA patients lacking the SMN gene, 10 asymptomatic parents, and 15 control subjects. We amplified mRNA fragments containing exon 7 of the SMN or BCD genes using reverse transcription-polymerase chain reaction since the transcript lacking exon 7 encodes a putative protein with a different C-terminal end. We used glyceraldehyde-3-phosphate dehydrogenase (GAPDH) transcript as an internal control, and the relative expression level of the SMN or BCD gene was shown as the ratio of SMN or BCD transcript to GAPDH transcript (S/G ratio). The mean S/G ratios of the patients were significantly lower than that of the parents and controls. However, among the patients examined in this study, there was no relationship between the S/G ratios and phenotypes of SMA. The results showed that the BCD gene expression was not related to the phenotypes of SMA. Furthermore, there was an overlap between the S/G ratios in patients and controls. As our discrimination study showed that the S/G ratio reflected the expression of the BCD transcripts in patients and the SMN transcripts in controls, this finding suggested that the BCD gene expression per se does not compensate for the loss of the SMN gene.

Adolescent↗
PubMed1997

Role of platelets in myocardial ischemia-reperfusion injury in dogs.

We investigated the involvement of circulating platelets in myocardial ischemia-reperfusion injury in canine autoperfused heart-lung preparations using filters to deplete platelets and/or leukocytes. The left anterior descending (LAD) coronary artery was occluded for 40 min, followed by 40 min reperfusion, in 3 groups: a leukocyte-platelet-depleted (LPD) group, in which both leukocytes and platelets were depleted; a leukocyte-depleted (LD) group, in which leukocytes alone were depleted; and a control group. There were no differences in hemodynamics or arrhythmias among groups before or during coronary occlusion. After reperfusion, the maximum rate of change in left ventricular pressure during systole and diastole was significantly higher in the LPD group than in the control and LD groups. The LPD group also showed gradual recovery of regional myocardial function and a decrease in the frequency of premature ventricular contractions. The LD group showed a slight improvement in cardiac function and arrhythmias compared with the control group. Although there was no significant difference in the pulmonary arterial plasma level of thromboxane B2 at any stage among groups, the control group showed an increase after reperfusion. These results suggest that platelets are important in reperfusion injury and that the depletion of both leukocytes and platelets effectively protects against reperfusion injury.

Animals↗
PubMed1997

Nonadrenergic, noncholinergic relaxation in longitudinal muscle of rat jejunum.

The mediators of nonadrenergic, noncholinergic (NANC) relaxation in the longitudinal muscle of rat jejunum were studied in vitro. Electrical field stimulation (EFS) of segments of rat jejunum induced a rapid transient relaxation followed by a subsequent contraction in the presence of atropine and guanethidine. NG-Nitro-L-arginine (L-NOARG, 10 microM) inhibited the EFS-induced NANC relaxation by about 25%, and L-arginine (1 mM) completely reversed this inhibition. Exogenously added nitric oxide (0.1-10 microM) induced relaxation of the segment. Treatment of the segment with alpha-chymotrypsin resulted in about 50% inhibition of the EFS-induced relaxation. Several peptide candidates for the mediator of NANC relaxation were examined by using selective antagonists of their receptors or by a receptor-desensitization method. Results indicated that vasoactive intestinal peptide, pituitary adenylate cyclase activating peptide, peptide histidine isoleucine, atrial natriuretic peptide and neurotensin are not associated with NANC relaxation of the segments. On the other hand, apamin at 1 microM inhibited the EFS-induced relaxation by 74%. Inhibitory effects of L-NOARG and, apamin or alpha-chymotrypsin treatment on the EFS-induced relaxation were additive and almost complete. Exogenous nitric oxide-induced relaxation was not affected by apamin. Inhibitory junction potentials (i.j.p.'s) were recorded from longitudinal muscle cells of rat jejunum. Apamin at 200 nM abolished i.j.p.'s induced by two pulses of EFS. These results suggest that NANC relaxation in longitudinal muscle of rat jejunum involves two independent components: one is a nitric oxide-mediated minor component, and the other is an unknown substance-mediated apamin-sensitive major component that is inhibited by alpha-chymotrypsin treatment.

Adrenergic Fibers↗
PubMed1997

Muscarinic autoinhibition and modulatory role of protein kinase C in acetylcholine release from the myenteric plexus of guinea pig ileum.

The modulatory role of protein kinase C on phospholipase A2, activation of which had been suggested to result in acetylcholine release from cholinergic neurons, was studied in longitudinal muscle preparations with the myenteric plexus of guinea pig ileum. The relationship of muscarinic autoinhibition to the modulation was also examined. Phorbol-12,13-dibutyrate (PDBu), an activator of protein kinase C, dose-dependently increased spontaneous and electrical field stimulation-induced acetylcholine releases from the preparation. The inhibitors of protein kinase C, staurosporine and calphostin C, inhibited the stimulatory effects of PDBu, but neither inhibitor affected spontaneous or electrical field stimulation-induced acetylcholine release in the absence of PDBu. On the other hand, atropine significantly increased electrical field stimulation-induced release by blocking a muscarinic autoinhibitory mechanism. Under the auto-inhibition blocked condition, U73122, an inhibitor of phospholipase C, and staurosporine significantly inhibited the effect of atropine on electrical field stimulation-induced release. An inhibitor of phospholipase A2, mepacrine, inhibited PDBu-induced acetylcholine release and also inhibited the effect of atropine on electrical field stimulation-induced release. An activator of phospholipase A2, melittin, and a product of the phospholipase, arachidonic acid, increased the spontaneous and electrical field stimulation-induced releases. These results suggest that the phospholipase C-protein kinase C system modulates acetylcholine release from cholinergic neurons by activating phospholipase A2 in the myenteric plexus of guinea pig ileum, and the activation of muscarinic autoreceptor may negatively modulate acetylcholine release at a point upstream of the system.

Acetylcholine↗
PubMed1997

Characterization of antimuscarinic effect of cimetropium bromide in guinea pig ileum.

Pharmacological characteristics of cimetropium bromide (cimetropium), a muscarinic receptor antagonist, were studied in longitudinal muscle preparations with myenteric plexus of guinea-pig ileum. Cimetropium was shown to have more potent antimuscarinic effect than butylscopolamine in inhibition of contraction of the preparations. Interestingly, when the inhibitory effects of cimetropium were compared in respect of relative potency to atropine between its effects on electrical field stimulation or nicotine-, and exogenous ACh-induced contraction, it has a more potent effect on the former contraction than that on the latter one. In the superfusion experiments of the preparation which had been preloaded with labelled choline, cimetropium decreased the labelled ACh release induced by electrical field stimulation under the muscarinic autoinhibition blocked-condition. From these findings, two pharmacologically characteristic effects of cimetropium in addition to post-synaptic muscarinic receptor antagonism were suggested: one is a weak effect on muscarinic autoreceptors in comparison to atropine and the other is an inhibitory effect on the ACh release.

Acetylcholine↗
PubMed1997

[The studies of extracorporeal shock wave lithotripsy (ESWL) for pancreatic ductal stones].

30 patients with main pancreatic duct stones were treated by ESWL. In 18 of 22 patients who had not previously undergone endoscopic pancreatic sphincterotomy (EPST) or endoscopic sphincterotomy (EST), the stone fragments disappeared after ESWL. The fragments were removed endoscopically in the remaining 4 cases. Complete clearance was achieved in 8 cases with endoscopically unextractable stones by ESWL. After the ESWL procedure, absolute relief from pain was reported by in 19 of 22 patients with abdominal complaints. Serum amylase levels decreased significantly, and dilatation of the main pancreatic duct (MPD) was reduced. In the medium-term follow-up period, pancreatic exocrine function and endocrine function had a possibility to be preserved. One case of pancreatic cancer and one case of an intraductal papillary tumor of the pancreas were found, indicating that careful observation is necessary even after complete removal of pancreatic stones. In cases of Santorini duct dominant, multiple stones, or stricture of the MPD, ESWL should be combined with EPST and endoscopic stenting for preventing recurrence of acute pancreatitis and pancreatic stones. In conclusion, ESWL is the first choice of treatment for pancreatolithiasis and useful procedure and the limited complications.

Adult↗
PubMed1997

Magnetic resonance cholangiography in hepatolithiasis.

OBJECTIVES: Our objective was to examine the usefulness of magnetic resonance cholangiography in hepatolithiasis. METHODS: Ten patients with hepatolithiasis were studied by ultrasonography, computed tomography, direct cholangiography, and magnetic resonance cholangiography to detect stones and to determine the morphological features of the bile ducts. In nine patients who underwent surgery, dilation and stenosis of the bile ducts were confirmed by intraoperative cholangioscopy, pathology, or both. RESULTS: Stones were demonstrated in seven patients by ultrasonography, in eight by computed tomography, in seven by direct cholangiography, and in all by magnetic resonance cholangiography. The locations of stones were identified in four patients by ultrasonography, in seven by computed tomography, in six by direct cholangiography, and in nine by magnetic resonance cholangiography. Among nine patients with dilation of the bile ducts, the dilation was shown by ultrasonography in seven, by computed tomography in eight, by direct cholangiography in six, and by magnetic resonance cholangiography in eight. Among seven patients with stenosis of the bile ducts, this stenosis was shown by direct cholangiography in four and by magnetic resonance cholangiography in six. Ultrasonography and computed tomography did not show the stenosis. Sensitivity for detection of biliary stenosis was significantly higher in magnetic resonance cholangiography. CONCLUSIONS: This study shows that magnetic resonance cholangiography not only detects stones, but can also delineate detailed information on the bile ducts, which is useful in the planning of treatment for hepatolithiasis.

Adult↗
PubMed1996

Ca(2+)-independent fusion of synaptic vesicles with phospholipase A2-treated presynaptic membranes in vitro.

To clarify the mechanism of exocytosis in neurotransmitter release, the fusion of synaptic vesicles with presynaptic membranes prepared from rat brain synaptosomes and concomitant acetylcholine (ACh) release induced by fusion of them were studied in vitro. Fusion of the synaptic vesicles with presynaptic membranes was measured by a fluorescence-dequenching assay with octadecyl rhodamine B. Synaptic vesicles fused with presynaptic membranes which had been pretreated with porcine phospholipase A2 (PLA2) in the presence of 20 microM Ca2+ and released ACh, whereas synaptic vesicles did not interact with non-pretreated membranes. The fusion followed by ACh release depended (i) on the activity of PLA2 during the membrane pretreatment, (ii) on the amount of pretreated membrane and (iii) on the duration of the pretreatment. The presence of Ca2+ ions during the pretreatment was essential for inducing a fusogenic activity of the membranes, but Ca2+ ions were not required for the fusion itself because the fusion experiment was carried out in the presence of 5mM EGTA without added Ca2+. The presence of quinacrine, an antagonist of PLA2, during the membrane pretreatment inhibited their fusogenic activity, suggesting the importance of activation of PLA2. Presence of albumin during the pretreatment, which is an adsorbent of free fatty acids, also inhibited the fusogenic activity. Arachidonic acid, when added during the pretreatment, potentiated the fusogenic activity of the membrane. These findings suggest that the conformational change in the presynaptic membrane phospholipids induced by PLA2 and the presence of arachidonic acid produced by PLA2 are important in the process of fusion of synaptic vesicles with the presynaptic membranes of rat brain, and that the fusion process itself is independent of Ca2+.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1996

Complete structure of the human alpha-albumin gene, a new member of the serum albumin multigene family.

The nucleotide sequence of the human alpha-albumin gene, including 887 bp of the 5'-flanking region and 1311 bp of the 3-flanking region (24,454 in total), was determined from three overlapping lambda phage clones. The sequence spans 22,256 bp from the cap site to the polyadenylylation site, revealing a gene structure of 15 exons separated by 14 introns. The methionine initiation codon ATG is within exon 1; the termination codon TGA is within exon 14. Exon 15 is entirely untranslated and contains the polyadenylylation signal AATAAA. The deduced polypeptide chain is composed of a 21-amino-acid leader peptide, followed by 578 amino acids of the mature protein. There are seven repetitive DNA elements (Alu and Kpn) in the introns and 3-flanking region. The sizes of the 15 alpha-albumin exons match closely those of the albumin, alpha-fetoprotein, and vitamin D-binding protein genes. The exons are symmetrically placed within the three domains of the individual proteins, and they share a characteristic codon splitting pattern that is conserved among members of the gene family. The results provide strong evidence that alpha-albumin belongs to, and most likely completes with, the serum albumin gene family. Based on structural similarity, alpha-albumin appears to be most closely related to alpha-fetoprotein. The complete structure of this family of four tandemly linked genes provides a well-characterized approximately 200 kb locus in the 4q subcentromeric region of the human genome.

Albumins↗