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Biomedical subjects

T Yoshimura

Publications and source records attributed to T Yoshimura.

At least 577 records · Page 32Linked to original sources
PubMed1989

Leucine zipper structure of the protein CRE-BP1 binding to the cyclic AMP response element in brain.

By screening a lambda gt11 library with the multimerized sequence of the cAMP response element (CRE), we isolated human clones encoding the CRE binding protein, CRE-BP1, from a human brain cDNA library. CRE-BP1 expressed in Escherichia coli bound not only to the CRE element of the somatostatin and fibronectin genes, but also to the CRE element of the adenovirus E4 gene, suggesting that the protein was not distinguishable from the adenovirus transcription factor, ATF. The human CRE-BP1 clone encoded a 54.5 kd protein similar at its carboxy terminus to the leucine zipper motifs found in other enhancer binding proteins such as C/EBP and c-jun/AP-1. CRE-BP1 mRNA was expressed in all of the cells examined and was abundant in brain. The structure of CRE-BP1 and its recognition elements suggest that cellular response to extracellular stimuli is controlled by a family of transcription factors that bind to related cis-active elements and that contain several highly conserved domains.

Activating Transcription Factor 2↗
PubMed1989

Familial myopathy with scapulohumeral distribution, rigid spine, cardiopathy and mitochondrial abnormality.

A 37-year-old woman with scapulohumeral muscular atrophy, rigid spine and cardiopathy is reported. Muscle weakness, advanced atrioventricular block and contractures at the neck, elbows and ankles had occurred during her childhood. An autosomal dominant mode of inheritance was suggested because her mother, sister and brother had the same disorder. Pleomorphic mitochondria had accumulated in the subsarcolemmal space of the skeletal muscle. There was no evident enzyme defect in the mitochondrial electron transport system. Although the clinical features had some similarity with those of Emery-Dreifuss muscular dystrophy or rigid spine syndrome, the pattern of inheritance and the muscle pathology differed.

Adult↗
PubMed1989

Radioimmunoassay for erythropoietin using anti-recombinant erythropoietin antibody with high affinity.

A sensitive radioimmunoassay (RIA) for the detection of erythropoietin (EPO) was developed using anti-recombinant EPO antibody with high affinity. The sensitivity was 100 amol/tube (5 mIU/ml) and it was possible to detect a serum EPO level between 5 and 200 mIU/ml. This method enabled us to measure native EPO as well as recombinant EPO. With this method we determined serum EPO levels in healthy individuals and patients with chronic renal disease, rheumatoid arthritis and iron deficiency anemia. Values in patients with chronic renal disease were lower than those in healthy individuals, while values in patients with rheumatoid arthritis, or iron deficiency anemia were significantly higher than those in healthy individuals.

Anemia, Hypochromic↗
PubMed1989

Three forms of monocyte-derived neutrophil chemotactic factor (MDNCF) distinguished by different lengths of the amino-terminal sequence.

Human monocyte-derived neutrophil chemotactic factor (MDNCF) was purified from culture supernatant of lipopolysaccharide-stimulated human peripheral blood mononuclear leukocytes on a column of Sepharose-bound murine monoclonal anti-MDNCF. About 65% of the culture fluid chemotactic activity was bound to the column. The unbound 35% probably represents chemotactic activity of other cytokines in the culture fluid. More than 85% of the bound activity was eluted by pH 2.5 glycine buffer. When this material was applied to an HPLC-CM column, gradient elution produced four well-separated A280 peaks, each of which had chemotactic activity. N-terminal amino acid analysis of the four peaks revealed three different sequences. One (MDNCF-c) was identical to the sequence that we reported previously. The other two (MDNCF-a and -b) had seven and five additional amino acids, respectively, at the N-terminus. MDNCF-a, -b and -c accounted for 8, 47 and 45% of the total MDNCF peptide. Alignment with the MDNCF cDNA sequence shows that MDNCF-a results from cleavage of a 20 residue signal peptide. MDNCF-c results from culture fluid proteolytic cleavage of the N-terminal sequences of MDNCF-a and -b at an R-S bond. The three peptides occurred in the four HPLC-CM peaks in different ratios. The bulk of any one peptide was distributed in two adjacent HPLC-CM peaks. This suggests that each peptide exists in a minimum of two states. In contrast to our previous multi-step purification, the immunoaffinity and HPLC-CM column sequence resulted in complete purification of MDNCF in two steps and led to identification of two additional MDNCF peptides, one of which has not heretofore been detected.

Amino Acid Sequence↗
PubMed1989

Neutrophil attractant/activation protein-1 (NAP-1) causes human basophil histamine release.

Basophils from five of six human donors released histamine in response to neutrophil attractant/activation protein-1 (NAP-1). Histamine release by this protein was concentration-dependent over the range of 3 x 10(-7) M to 4 x 10(-6) M. At 4 x 10(-6) M, the mean agonist-induced release was 16 +/- 3% (SEM) of total basophil histamine. For the same basophil preparations, release by anti-IgE was 35 +/- 6%. The chemotactic protein did not cause release of histamine from basophils at 0 degrees C or in the presence of 10 mM EDTA. The time-course of histamine release was rapid; release was 43% of maximal after 30 s and maximal after 1 min of incubation. Thus, in addition to its previously characterized neutrophil chemotactic and activating properties, this protein activates human basophils.

Basophils↗
PubMed1989

Inflammatory fibrous histiocytoma presenting leukemoid reaction.

A case of inflammatory fibrous histiocytoma presenting leukemoid reaction is reported. A tumor had developed at the right scapular region 10 years ago and recurred twice with fever and leukocytosis, and finally with leukemoid reaction. Besides the histopathological features typical of malignant fibrous histiocytoma, this tumor showed prominent and diffuse infiltration of neutrophilic leukocytes. Hematologic examination of the bone marrow aspirates disclosed myeloid hyperplasia. Bacteriological examination revealed no pathogenic microorganisms in the tumor tissue. Chemotactic activity of the neutrophilic leukocytes was demonstrated in the extract obtained from the tumor, and subcutaneous injection of the extract into rats induced myeloid hyperplasia in the bone marrow and neutrophil infiltration in the liver and spleen of the animals. These results suggest the possibility of the case as a colony-stimulating factor-producing tumor.

Aged↗
PubMed1989

Complete amino acid sequence of a human monocyte chemoattractant, a putative mediator of cellular immune reactions.

In a study of the structural basis for leukocyte specificity of chemoattractants, we determined the complete amino acid sequence of human glioma-derived monocyte chemotactic factor (GDCF-2), a peptide that attracts human monocytes but not neutrophils. The choice of a tumor cell product for analysis was dictated by its relative abundance and an amino acid composition indistinguishable from that of lymphocyte-derived chemotactic factor (LDCF), the agonist thought to account for monocyte accumulation in cellular immune reactions. By a combination of Edman degradation and mass spectrometry, it was established that GDCF-2 comprises 76 amino acid residues, commencing at the N terminus with pyroglutamic acid. The peptide contains four half-cystines, at positions 11, 12, 36, and 52, which create a pair of loops, clustered at the disulfide bridges. The relative positions of the half-cystines are almost identical to those of monocyte-derived neutrophil chemotactic factor (MDNCF), a peptide of similar mass but with only 24% sequence identity to GDCF. Thus, GDCF and MDNCF have a similar gross secondary structure because of the loops formed by the clustered disulfides, and their different leukocyte specificities are most likely determined by the large differences in primary sequence.

Amino Acid Sequence↗
PubMed1989

Production and characterization of recombinant human neutrophil chemotactic factor.

A putative mature human neutrophil chemotactic factor (NCF) corresponding to the C-terminal 72 amino acids of its precursor was directly produced in Escherichia coli by recombinant DNA technology. Human NCF was present in both the soluble and insoluble protein fractions of the homogenate of host cells, and it was partially purified as a water-soluble polypeptide from both fractions, separately. The partially purified NCF preparation was highly purified to an endotoxin-free homogeneous polypeptide by means of CM-Sepharose CL-6B column chromatography and gel filtration on Toyopearl HW-55. No difference between the human NCF preparations purified from both starting materials could be found concerning purity, primary structure, solubility, molecular weight, and chemotactic activity for human neutrophils. The amino acid sequence of recombinant human NCF was identical to the sequence deduced from the cDNA sequence. A methionine residue due to the translation initiation codon was removed. Recombinant human NCF was found to be biologically active and to exhibit chemotactic activity for human neutrophils in vitro and cause a neutrophil infiltration in vivo in mice.

Amino Acid Sequence↗
PubMed1989

Role of substrate in reversible activation of proteasomes (multi-protease complexes) by sodium dodecyl sulfate.

Previously, we reported that proteasomes (large multi-protease complexes) are present in a latent state in a variety of eukaryotic cells, and can be activated by treatment with various compounds such as sodium dodecyl sulfate (SDS) or poly-lysine (Tanaka et al. (1988) J. Biol. Chem. 263, 16209-16217). In the present study, the mechanism of activation of latent proteasomes by SDS was examined. Latent proteasomes were greatly activated by addition of low concentrations of 0.04 to 0.08% SDS in the presence of substrate. This activation appeared to be reversible, because SDS-activated proteasomes returned to a latent state when the concentration of SDS was reduced by dilution. In contrast, in the absence of substrate, latent proteasomes lost their activity almost completely in an irreversible fashion within a few minutes during treatment with SDS at either 0 or 37 degrees C. Interestingly, SDS-treated proteasomes were markedly protected against this rapid inactivation by either a peptide or protein substrate. Moreover, removal of the substrate after activation of proteasomes caused their rapid irreversible inactivation. These results indicate that the substrate is necessary for reversible activation of latent proteasomes by SDS. This effect of substrate is presumably important in regulation of intracellular protein breakdown by activated proteasomes in eukaryotic cells.

Cysteine Endopeptidases↗
PubMed1989

Decreased fatty acylation of myelin proteolipid protein in the twitcher mouse.

We examined chronological changes of myelin proteins of the brainstem and spinal cord of the twitcher mouse (15, 20, and 30 days old), a murine model of human globoid cell leukodystrophy caused by a genetic deficiency of galactosylceramidase I activity. The yield of myelin was normal until postnatal day 20, whereas galactosylsphingosine (psychosine) accumulated with age in myelin. The protein profiles of myelin and the activity of 2',3'-cyclic nucleotide 3'-phosphodiesterase in the myelin remained normal throughout the experimental period. Fatty acylation of proteolipid protein (PLP) was examined in a cell-free system by incubation of myelin with [3H]palmitic acid, CoA, and ATP, and was normal at postnatal day 15, but decreased after postnatal day 20. Decreased fatty acylation of PLP was also observed in the twitcher mouse at postnatal day 20 when the isolated myelin was incubated with [14C]palmitoyl-CoA in the absence of ATP and CoA, or the slices of brainstem and spinal cord were incubated with [3H]palmitic acid. The activity of fatty acid:CoA ligase was reduced in myelin. These data suggest that decreased acylation of PLP in twitcher mouse myelin is probably due to reduced activities for both activation and transfer of fatty acid into PLP and that metabolic disturbance is present in myelin because acylation of PLP has been shown to occur in myelin membrane. Although psychosine (200 microM) inhibited only 17% of the acylation in vitro, it may be responsible for the reduced acylation of PLP in vivo.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1989

Effect of galanin on glucose-, arginine-, or potassium-stimulated insulin release.

We have examined the effect of galanin infusion on glucose-stimulated release of insulin from the isolated perfused pancreas of the rat to better characterize the effect of galanin on the first and second phases of insulin release. The effects of galanin on insulin release stimulated by L-arginine or high concentrations of potassium were also examined. When perfusion of galanin was started 4 min before the start of perfusion of high glucose (16.7 mM), galanin (10(-8)-10(-11) M) inhibited both the first and second phases of insulin release in a dose-dependent manner. When perfusion of galanin (10(-8) or 10(-9) M) was started simultaneously with high glucose (16.7 mM), only the second phase of insulin release was suppressed (P less than 0.05). Galanin (10(-9) M) failed to inhibit insulin release stimulated by L-arginine (10 and 5 mM) or potassium (25 and 20 mM). These findings suggest that the inhibitory action of galanin on glucose-stimulated insulin release is exerted on early intracellular events that occur during the stimulation of insulin release and that are common to both phases. Because galanin does not inhibit insulin release stimulated by L-arginine or potassium, galanin may inhibit glucose-stimulated closure of potassium channels.

Animals↗
PubMed1989

Diagnostic significance of IgG, C3, and C9 at the limb muscle motor end-plate in minimal myasthenia gravis.

We detected deposits of IgG, C3, and C9 (immune complexes) at the limb muscle motor end-plates (biceps brachii muscle) in 16 of 19 patients who exhibited only ocular signs and symptoms of myasthenia gravis that were improved by intravenous injections of edrophonium chloride. Circulating anti-acetylcholine receptor (anti-AChR) antibodies were negative in 6 of the 16 patients, but the motor end-plate fine structure in the postsynaptic regions was abnormal in all 16. Single-fiber EMG revealed no abnormalities in 8 of 13 patients studied. Our results indicate that the detection of immune complexes at the limb muscle end-plate provides a highly sensitive and confirmative method for diagnosing patients with minimal or atypical myasthenia gravis who have no detectable anti-AChR antibodies in their serum.

Adolescent↗
PubMed1989

[Activity of serum arylsulfatase B in nasal allergy patients].

Although the arylsulfatase B has been reported to inactivate slow reacting substance of anaphylaxis (SRS-A) in vitro there has not been studied about the relation between this enzyme and nasal allergy in vivo. The present study was done to examine the serum level of arylsulfatase B in 73 nasal allergy patients and 13 normal controls. Serum arylsulfatase activity was quantified by measurement of the hydrolysis product (p-nitrocatechol) generated by the interaction of this enzyme and a substrate (p-nitrocatechol sulfate, Sigma). The results are summarised as follows; 1. Arylsulfatase B activity is significantly elevated in sera of nasal allergy patients than in that of normal subjects. 2. There are no correlation between the enzyme activity and the number of peripheral blood eosinophiles. 3. There is tendency the severe the nasal obstruction, the lower the level of the enzyme activity.

Chondro-4-Sulfatase↗
PubMed1989

[Acute disseminated encephalomyelitis affecting medulla and upper cervical cord--comparison of the clinical signs and MRI findings].

Correlation of MRI abnormalities and clinical manifestations was studied in a case of acute disseminated encephalomyelitis. A 54-year-old man developed Brown-Séquard syndrome affecting the right upper cervical cord, bilateral bulbar palsy, right Horner syndrome, and rotatory nystagmus. After the admission, right facial numbness and weakness of left upper and lower limbs were added. He was treated with glucocorticosteroid successfully. Painful tonic seizures of left upper and lower limbs were noted in the convalescence. T1-weighted MRI of the brain and spinal cord revealed low signal intensity areas in the medulla oblongata and right upper cervical cord. T2-weighted images showed a high signal intensity in the same areas. The distribution of MRI abnormalities well corresponded to the clinically expected lesions. The MRI abnormalities gradually decreased and disappeared with his recovery. The MRI abnormalities appeared to reflect edema accompanying the acute inflammatory process. MRI seems to be a very useful test for verifying lesions in the brainstem and spinal cord in a case of acute disseminated encephalomyelitis.

Acute Disease↗