Internal transport barrier on q=3 surface and poloidal plasma spin up in JT-60U high- beta p discharges.
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Journal Article↗
Biomedical subjects
S Tsuji
Publications and source records attributed to S Tsuji.
Expression cloning of a GM3-specific alpha-2,8-sialyltransferase (GD3 synthase).
A cDNA encoding a GM3-specific alpha-2,8-sialyltransferase (GD3 synthase) was obtained from an expression cDNA library of human melanoma cell line WM266-4 by enrichment of Namalwa KJM-1 cells highly expressing GD3 using an anti-GD3 antibody and a fluorescence-activated cell sorter. Selection of B-cell line Namalwa cells expressing transfected cDNAs in the presence of anti-GD3 monoclonal antibody KM641 gave a cDNA (pAMo-GD3) encoding a protein with a type II transmembrane topology as found for mammalian glycosyltransferases. The following evidence confirms that the cDNA encodes an alpha-2,8-sialyltransferase, which specifically converts GM3 to GD3. (i) Transfection of pAMo-GD3 into Namalwa KJM-1 cells leads to the appearance of GD3 and a GD3 synthase activity. (ii) Northern blot analysis revealed a correlation between the expression of this gene and GD3 in several cell lines. (iii) The putative COOH-terminal active domain of this cloned enzyme fused with protein A has been purified with IgG-Sepharose beads and has been shown to possess GD3-synthesizing activity, excluding the possibility that the cloned cDNA encodes a transacting factor inducing a GD3 synthase. The deduced primary sequence also contains the "sialyl motif" conserved among all the sialyltransferases cloned to date. The polymerase chain reaction analysis reveals that this gene is located on chromosome 12.
Amino Acid Sequence↗
[A case of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) associated with acute bilateral optic neuritis with normal findings on pattern-reversal visual evoked potential study].
A 35-year-old man with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) associated with acute bilateral optic neuritis is described. At age 33, he noticed a tingling sensation in his toes followed by weakness in the lower limbs. He was admitted to our hospital because he became unable to walk without support. His motor and sensory symptoms gradually resolved during 7 months admission only with physical rehabilitation. At age 35, in July 1988, he noticed a tingling sensation in his toes and fingers, which reached to the knees and elbows in October 1988, when he developed weakness in the lower limbs. Motor and sensory symptoms were almost stationary thereafter and in March 1989, he experienced bilateral blurred vision of acute onset without ocular pain. He was readmitted to our hospital in April 1989. The neurological examination revealed decreased visual acuity of both eyes without any abnormality of the optic disks, mild weakness on flexion and extension of toes, an absence of Achilles reflex, and distal impairment of pain and touch sensations in the upper limbs, and of pain, touch and vibration sensations in the lower limbs. After laboratory examinations, CSF protein was elevated (122 mg/dl), and sensory nerve conduction velocity of the right median nerve was decreased (37.1 m/sec). The sural nerve action potential was not elicited on electrical stimulation. Central scotoma was found in both eyes by the visual field examination. P100 latency was seen to be normal by repeated pattern-reversal visual evoked potential (VEP) studies. CT and MRI of the brain were unremarkable.(ABSTRACT TRUNCATED AT 250 WORDS)
Acute Disease↗
Kinetic properties and acceptor substrate preferences of two kinds of Gal beta 1,3GalNAc alpha 2,3-sialyltransferase from mouse brain.
The cDNAs encoding two kinds of Gal beta 1,3GalNAc alpha 2,3-sialytransferases (ST3GalA.1 and ST3GalA.2) have been cloned from mouse brain, both of which could synthesize the NeuAc alpha 2,3Gal beta 1,-3GalNAc sequence of gangliosides as well as O-glycosidically linked oligosaccharides of glycoproteins [Lee et al. (1993) Eur. J. Biochem. 216, 377-385; Lee et al. (1994) J. Biol. Chem. (in press)]. Kinetic analysis of the two sialyltransferases using Gal beta 1,3GalNAc, asialoGM1, or asialofetuin revealed that ST3GalA.1 exhibits the highest Km value for asialoGM1 (Km = 1.25 mM) and the lowest one for asialofetuin (Km = 0.10 mM), whereas the Km values of ST3GalA.2 for the substrates are very similar (Km approximately 0.5 mM). The synthesis of GM1b from asialoGM1 by ST3GalA.1 was clearly inhibited in the presence of Gal beta 1,3GalNAc or asialofetuin, but that by ST3GalA.2 was not at all. On the other hand, the activity of ST3GalA.2 toward Gal beta 1,3GalNAc or asialofetuin was inhibited by asialoGM1 or GM1. The results of acceptor competition experiments involving asialoGM1, Gal beta 1,3GalNAc, and asialofetuin indicated that ST3GalA.2 exhibits noncompetitive inhibition between asialoGM1 and Gal beta 1,3GalNAc or between asialoGM1 and asialofetuin, whereas ST3GalA.1 exhibits competitive inhibition between all kinds of acceptors. These results strongly indicate that acceptor preference of ST3GalA.1 is different from that of ST3GalA.2, although their acceptor substrate specificities are the same; i.e., gangliosides serve as predominant acceptors for the latter over O-glycosidically linked oligosaccharides of glycoproteins, which are much better acceptors for the former.
Animals↗
A single stage posterior approach and rigid fixation for preventing kyphosis in the treatment of spinal tuberculosis.
STUDY DESIGN: The authors employed a new mode of treatment for spinal tuberculosis consisting of single stage posterior instrumentation and fusion without anterior debridement. Ten patients were operated upon in this manner. Chemotherapy was instituted 2 weeks preoperatively and continued for a mean period of 11 months. Cotrel-Dubousset or a comparable system was used for fixation. OBJECTIVES: Patients were followed for 3 monthly intervals with serial anteroposterior and lateral x-rays, erythrocyte sedimentation rate, physical examination, and patients' self reports. The mean follow up period was 24.2 months (range, 17-36 months). METHODS: Measurement of kyphosis angle in the lateral x-ray view was used to evaluate treatment. RESULTS: Only a 3.4 degrees mean loss of correction was observed over the follow-up period. All patients were satisfied. CONCLUSION: Our results show that posterior rigid fixation and chemotherapy provide satisfactory stabilization, reduce surgical morbidity, and prevent development of late kyphosis in selected patients with Pott's disease of the thoracolumbar spine.
Antitubercular Agents↗
Increased expression of c-met messenger RNA following acute gastric injury in rats.
The aim of the present study was to evaluate messenger RNA expression of c-met, a hepatocyte growth factor receptor gene, after gastric mucosal injury in rats. Male Sprague-Dawley rats were fasted for 24 hours, received 0.6 N hydrochloric acid (HCl), and served for polyadenylated RNA extraction from the oxyntic gastric mucosa. The transcripts of rat c-met gene were analyzed by reverse-transcript polymerase chain reaction and Northern blotting. Although it was detected even before the HCl administration, the c-met expression increased 6, 24 and 48 hours after the HCl administration. Thereafter, gastric mucosal injury diminished and the c-met expression declined. Hepatocyte growth factor reportedly plays an important role in gastric cell proliferation. The increased c-met expression indicates that this gene may participate in the healing process of gastric mucosa after injury.
Amino Acid Sequence↗
Comparison of benzodiazepine receptor and regional cerebral blood flow imaging of epileptiform foci in hippocampal kindled rabbits: a study with in vivo double tracer autoradiography using 125I-iomazenil and 99mTc-HMPAO.
To clarify experimentally whether benzodiazepine (Bz) receptor or regional cerebral blood flow (rCBF) imaging is more sensitive in the detection of epileptic foci, we simultaneously examined the Bz receptor and rCBF distribution changes in hippocampal kindled rabbits with in vivo double tracer autoradiography using 125I-labeled Ro 16-0154 (125I-Iomazenil) and 99mTc-labeled hexamethylpropylene amine oxime (99mTc-HMPAO). In visual and quantitative analyses, 125I-Iomazenil accumulation in brain slices extracted after the completion of the kindling was markedly and extensively decreased in the kindled right CA1 region, and further in the right temporal lobe, dentate gyrus, CA2, CA4, and bilateral CA3 regions, regarded as the propagated sites of seizure discharges. 99mTc-HMPAO accumulation was much more slightly and less extensively decreased in the right CA1, frontal, temporal and dentate gyri. Further, this decrease in 125I-Iomazenil accumulation was not due to neuropathological abnormalities, which consisted only of tissue damage corresponding to electrode track in the CA1. Both the kindled and propagated sites are known to have a possibility of acquiring epileptogenesis as experimental epileptic foci. These results suggest that Bz receptor imaging is much more sensitive in the detection of epileptic foci than rCBF imaging, and therefore that Bz receptor imaging is useful in clinical epilepsy.
Animals↗
Cloning and expression of cDNA for a new type of Gal beta 1,3GalNAc alpha 2,3-sialyltransferase.
Based on the sequences of the highly conserved segments in the previously cloned sialyltransferases, a cDNA encoding a new type of Gal beta 1,3GalNAc alpha 2,3-sialyltransferase (ST3GalA.2) has been isolated from both mouse and rat brain cDNA libraries. The cDNA sequences included an open reading frame coding for 350 amino acids, and the primary structure of this enzyme suggested a putative domain structure consisting of four regions, like that in other glycosyltransferases. The deduced amino acid sequence of ST3GalA.2 (mouse) showed 76% identity in the active domain with that of the previously cloned mouse Gal beta 1,3GalNAc alpha 2,3-sialyltransferase (ST3GalA.1 (Lee, Y.-C., Kurosawa, N., Hamamoto, T., Nakaoka, T., and Tsuji, S. (1993) Eur. J. Biochem. 216, 377-385)). Northern blotting indicated that the expression of ST3GalA.2 mRNA is tissue-specific, it being prominent in brain and liver, while that in the other tissues is very low. This enzyme expressed in COS-7 cells exhibited transferase activity only toward the disaccharide moiety of Gal beta 1,3GalNAc of glycolipids as well as glycoproteins and oligosaccharides like ST3GalA.1, but showed a difference in acceptor substrate preference, i.e. asialo-GM1 and GM1 were much more suitable substrates for ST3GalA.2 than for ST3GalA.1.
Amino Acid Sequence↗
Decay-accelerating factor on human umbilical vein endothelial cells. Its histamine-induced expression and spontaneous rapid shedding from the cell surface.
Decay-accelerating factor (DAF) is a membrane protein that protects host cells from attack by its own complement. Although DAF expression on endothelial cells is thought to increase pathophysiologically, little is known about the natural mediators that modulate DAF expression on endothelial cells. In this study, we evaluated the effect of histamine on DAF expression on human umbilical vein cells (HUVEC). HUVEC were cultured with histamine, and DAF expression on HUVEC was determined by flow cytometry after immunostaining with a mAb to DAF. DAF expression on HUVEC was increased at 10 microM histamine, and the final level was increased time-dependently by 150% to 200% after a 24-h incubation with 100 microM histamine. The histamine-induced DAF expression was inhibited by actinomycin D and cycloheximide and accompanied by an increase in the DAF mRNA level, indicating that both transcription and translation are required. In addition, the histamine-induced DAF expression was inhibited by pyrilamine, an H1 blocker, but not by cimetidine, an H2 blocker, indicating that histamine induces the DAF expression through H1 receptors. We also demonstrated that the turnover of DAF is faster than that of MCP and CD59, and DAF is released into the culture supernatant. DAF is a glycosylphosphatidylinositol-linked protein that is released from HUVEC by a phosphatidylinositol-specific phospholipase C. Although HUVEC also contain the glycosylphosphatidylinositol-anchored complement inhibitor CD59, this was not released during a 24-h incubation, suggesting that the shedding of DAF from HUVEC is not caused by PI-PLC but by other enzymes, possibly proteinases. These results suggest that histamine, which is released from mast cells and basophils by complement-derived anaphylatoxins, increases the complement defense ability of endothelial cells by increasing their levels of DAF expression.
Antigens, CD↗
Chromosome mapping of the human (RECA) and mouse (Reca) homologs of the yeast RAD51 and Escherichia coli recA genes to human (15q15.1) and mouse (2F1) chromosomes by direct R-banding fluorescence in situ hybridization.
We mapped the human (RECA) and mouse (Reca) homologs of the yeast RAD51 and Escherichia coli recA genes to human and mouse chromosomes by direct R-banding fluorescence in situ hybridization. This gene was assigned to human chromosome 15q15.1 and to mouse chromosome 2F1, respectively. This is the first report on the precise localization of this gene to human and mouse chromosomes. This gene was mapped to a region on human chromosome 15q15.1 and mouse 2F1 that is believed to be a conserved syntenic group.
Animals↗
Molecular cloning and expression of chick embryo Gal beta 1,4GlcNAc alpha 2,6-sialyltransferase. Comparison with the mammalian enzyme.
DNA clones encoding beta-galactoside alpha 2,6-sialyltransferase have been isolated from chick embryonic cDNA libraries using sequence information obtained from the conserved amino acid sequence of the previously cloned enzymes. The cDNA sequence revealed an open-reading frame coding for 413 amino acids, and the deduced amino acid sequence showed 57.6% identity with the sequence of rat liver Gal beta 1,4GlcNAc alpha 2,6-sialyltransferase. The primary structure of this enzyme suggested a putative domain structure, similar to structures found in other glycosyltransferases, consisting of a short N-terminal cytoplasmic domain, a signal-membrane anchor domain, a proteolytically sensitive stem region and a large C-terminal active domain. The identity of this enzyme was confirmed by construction of a recombinant sialyltransferase in which the N-terminus part including the cytoplasmic tail, signal anchor domain and stem region was replaced with an immunoglobulin signal peptide sequence. The expression of this recombinant protein in COS-7 cells resulted in secretion of a catalytically active and soluble form of the enzyme into the medium. The expressed enzyme exhibited activity only towards the disaccharide moiety of Gal beta 1,4GlcNAc in glycoproteins.
Amino Acid Sequence↗
Molecular cloning and expression of GalNAc alpha 2,6-sialyltransferase.
cDNA clones encoding GalNAc alpha 2,6-sialyltransferase (EC 2.4.99.3) have been isolated from chick embryo cDNA libraries using sequence information obtained from the conserved amino acid sequence of the previously cloned enzymes. The cDNA sequence included an open reading frame coding for 566 amino acids, and the deduced amino acid sequence showed 12% identity with that of Gal beta 1,4GlcNAc alpha 2,6-sialyltransferase from chick embryo. The primary structure of this enzyme suggested a putative domain structure, like that in other glycosyltransferases, consisting of a short NH2-terminal cytoplasmic domain, a signal-membrane anchor domain, a proteolytically sensitive stem region, and a large COOH-terminal active domain. The identity of this enzyme was confirmed by the construction of a recombinant sialyltransferase in which the NH2-terminal part (232 amino acid residues) was replaced with the immunoglobulin signal sequence. The expression of this recombinant in COS-7 cells resulted in secretion of a catalytically active and soluble form of the enzyme into the medium. The expressed enzyme exhibited activity toward only asialomucin and (asialo)fetuin, no significant activity being detected toward the other glycoprotein and glycolipid substrates tested. 14C-Sialylated glycols obtained from asialomucin re-sialylated with this enzyme were identical to NeuAc alpha 2,6-GalNAc-ol and GlcNAc beta 1,3(NeuAc alpha 2,6) GalNAc-ol. Synthetic GalNAc-SerNAc also served as an acceptor for alpha 2,6-sialylation. These results clearly showed that the expressed enzyme is GalNAc alpha 2,6-sialyltransferase.
Acetylgalactosamine↗
Endothelin-1 is involved in the pathogenesis of ischemia/reperfusion liver injury by hepatic microcirculatory disturbances.
Hepatic microcirculatory perturbation is observed after ischemia/reperfusion. Endothelin-1, a potent vasoconstrictive peptide, is known to modulate local circulation. This study was designed to examine whether endothelin-1 participates in the mechanism of microcirculatory disturbance and damage of the liver after ischemia/reperfusion. Ischemia in the median and left lateral lobes of the liver was induced for 60 min; it was followed by reperfusion for 24 hr. In some rats, endothelin-1 antiserum or control serum without endothelin-1-blocking activity was administered intravenously just before reperfusion. Rats were divided into three groups: an ischemia/reperfusion group that was injected with control serum, an endothelin-1 antiserum-treated group and a sham-operated group. Endothelin-1 concentrations in blood collected from the suprahepatic vena cava were measured before and after ischemia/reperfusion by use of a sandwich enzyme immunoassay. Index of blood volume in regional hepatic tissue and index of blood oxygenation in regional hepatic tissue were assessed with an organ reflectance spectrophotometry system before and at 5 min and 1, 2, and 24 hr after reperfusion. The endothelin-1 concentration in the ischemia/reperfusion group started to rise immediately at onset of reperfusion from basal values around 1 pg/ml and reached a value of 5 to 6 pg/ml 5 min after reperfusion; it was maintained at significantly high levels during the reperfusion period compared with the sham-operated group. Hepatic microcirculatory disturbance indicated by lowered index of blood volume in regional hepatic tissue and index of blood oxygenation in regional hepatic tissue levels was observed in the early phase of reperfusion in the ischemia/reperfusion group.(ABSTRACT TRUNCATED AT 250 WORDS)
Alanine Transaminase↗
Endogenous nitric oxide attenuates ethanol-induced perturbation of hepatic circulation in the isolated perfused rat liver.
The purpose of this study was to clarify the role of endogenous nitric oxide in ethanol-induced perturbation of microcirculation and hepatic injury in perfused rat liver. Infusion of ethanol into the portal vein at 25 and 100 mmol/L increased portal pressure, which is an indicator of hepatic vasoconstriction, in a concentration-dependent fashion. Portal pressure started to rise immediately after ethanol load, then decreased gradually and remained at higher than basal levels throughout the period of ethanol infusion. Release of lactate dehydrogenase into the effluent perfusate began to increase after 30 min of ethanol infusion and continued to increase during the 60-min period of ethanol infusion. The lactate dehydrogenase level in the effluent perfusate at 60 min was dependent on the ethanol concentration (0 mmol/L, 8 +/- 3 IU/L; 25 mmol/L, 16 +/- 2 IU/L; 100 mmol/L, 52 +/- 6 IU/L). Simultaneous infusion of NG-monomethyl-L-arginine, a nitric oxide synthesis inhibitor, enhanced significantly the ethanol-induced increase in portal pressure by 100% to 400% and increased lactate dehydrogenase release by 40% to 80%. The effect of NG-monomethyl-L-arginine on the ethanol-induced increase in portal pressure was completely reversed by the co-infusion of an excess dose of L-arginine. Change in portal pressure averaged over 60 min of ethanol infusion correlated with levels of lactate dehydrogenase release 60 min after the initiation of ethanol infusion (r = 0.77, p < 0.01). In conclusion, inhibition of the action of endogenous nitric oxide was associated with an increase in hepatic vasoconstriction and hepatocellular damage.(ABSTRACT TRUNCATED AT 250 WORDS)
Analysis of Variance↗
Effect of intravenous immunoglobulin in Lambert-Eaton myasthenic syndrome with small-cell lung cancer: correlation with the titer of anti-voltage-gated calcium channel antibody.
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Action Potentials↗
Role of cell surface O-linked oligosaccharides in adhesion of HL60 cells to fibronectin: regulation of integrin-dependent cell adhesion by O-linked oligosaccharide elongation.
The adhesion of the myelogenous leukemia cell line, HL60, to fibronectin and its fragments, heparin binding fragment (40 kDa) and cell attachment fragment (120 kDa), was enhanced by culturing with benzyl-alpha-GalNAc (BZ alpha GalNAc). Enhancement of cell adhesion to fibronectin was also observed on treatment of HL60 cells with 12-O-tetradecanoylphorbol 13-acetate (TPA). However, an additive effect of BZ alpha GalNAc and TPA treatments was not observed. The expression of VLA4 and VLA5 did not change during treatment with BZ alpha GalNAc or TPA. Cell adhesion to fibronectin before and after treatment with BZ alpha GalNAc or TPA was inhibited by anti-VLA4 and anti-VLA5 monoclonal antibodies. Staining of the cells with Helix pomatia lectin demonstrated that culturing of the cells with BZ alpha GalNAc blocked elongation of O-linked oligosaccharides on the cell surface and led to accumulation of GalNAc-O-Ser/Thr. Labeling of cell surface carbohydrates with [3H]-glucosamine followed by treatment with TPA revealed that O-glycosylated glycoproteins including CD43 were released from the cell surface during this treatment. These findings indicate that integrin-dependent cell adhesion, particularly VLA4- or VLA5-dependent cell adhesion, of HL60 cells is prevented with the extension of O-linked oligosaccharides and recovers with the disappearance of O-linked oligosaccharides from the cell surface.
Acetylgalactosamine↗
Mutational analysis of the amyloid precursor protein gene in Japanese familial Alzheimer's disease kindreds.
We sequenced the entire coding region of the amyloid precursor protein (APP) genes of 11 unrelated patients with Japanese familial Alzheimer's disease (FAD) in order to determine the exact frequency of known APP gene mutations and to search for novel mutations responsible for FAD. Three out of 11 (27.3%) FAD patients showed the known Val to Ile mis-sense mutation at codon 717, but no other mutations were detected in the entire coding region. Analysis of exons 16 and 17 in 30 Japanese with sporadic AD revealed no mutations. Moreover, there were no significant differences in the allele frequencies of the DNA polymorphism in intron 9 among the 11 FAD, 39 sporadic AD, and 110 control subjects.
Adult↗
Familial amyotrophic lateral sclerosis with a mutation in the Cu/Zn superoxide dismutase gene.
Several missense mutations within exons 1, 2, 4 and 5 of the gene for Cu/Zn-binding superoxide dismutase (SOD1) have been discovered to be involved in the development of chromosome 21q-linked familial amyotrophic lateral sclerosis (FALS). We describe here an autopsied patient with FALS, in whom we have recently identified a novel missense mutation in exon 1 of the SOD1 gene. The neuropathological findings were compatible with those described previously in patients with FALS with posterior column involvement. This suggests that mutations of the SOD1 gene may be responsible for this form of FALS.
Adult↗