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Biomedical subjects

T Shinohara

Publications and source records attributed to T Shinohara.

At least 271 records · Page 15Linked to original sources
PubMed1989

Size fractionation of oligosaccharides by liquid chromatography on a cation-exchange column.

Oligosaccharides, labelled with 2-aminopyridine at their reducing ends, were satisfactorily fractionated according to the sugar sizes on Shodex RSpak DC-613, a cation-exchange resin column (Na+ form), with water-acetonitrile as the eluent in the presence of sodium acetate or triethylammonium acetate buffer. For the fractionation of sugar samples, dextran hydrolyzates, chitin oligomers and oligosaccharide moieties of ovomucoid were used. The oligosaccharides were strongly adsorbed to the resin column with solvents containing less water and at lower temperature, and were eluted in order of increasing molecular size above the critical concentration of acetonitrile. Baseline separation of a dextran hydrolyzate up to oligomers having 20 glucose units was observed by gradient elution. The separation efficiency and elution pattern were investigated by changing the buffer concentration, mobile phase pH and temperature.

Chromatography, Ion Exchange↗
PubMed1989

Molecular mimicry. Yeast histone H3-induced experimental autoimmune uveitis.

Experimental autoimmune uveitis (EAU) serves as an animal model of ocular inflammation. The disease is caused by the immunization with microgram amounts of a soluble retinal protein, designated S-Ag, in susceptible animal strains, including primates. We induced EAU and pinealitis in Lewis rats with a small synthetic peptide, corresponding to amino acid positions 106 to 121 in yeast histone H3, which contains five consecutive amino acids identical to a uveitopathogenic site in human S-Ag. In addition, native yeast histone was also capable of inducing an EAU in Lewis rats. Lymph node cells from animals immunized with either peptide M (uveitopathogenic site of S-Ag), histone H3 peptide, or native histone showed significant cross-reaction. Also, we adoptively transferred the EAU in naive rats by lymph node cells. These findings provide a basis for studying autoimmune inflammatory diseases of the eye in humans.

Amino Acid Sequence↗
PubMed1989

Long-term prognosis of Kawasaki disease patients with coronary artery obstruction.

The prognosis of coronary artery obstruction was studied in patients with Kawasaki disease. Between May 1973 and December 1987, coronary artery obstruction was diagnosed by coronary angiography in 30 patients (21 males, 9 females), of whom, only 8 (26.7%) had clinical symptoms. One patient died after 9 years of illness. Two complained of frequent chest pain, which disappeared after bypass surgery in one case and spontaneously in the other. Five had symptomatic myocardial infarction. Myocardial ischemia was diagnosed in 31.8% by treadmill stress testing, but was well demonstrated in 85.7% by thallium-201 myocardial tomography. Frequent ventricular premature beats, Wenckebach-type atrioventricular block, and ST-segment depression accompanied by chest pain were recognized by 24-h Holter monitoring. In the past, the methods used to determine the prognosis of Kawasaki disease patients with coronary artery obstruction were not adequate. However, the examinations used in this study revealed an improved ability to determine the prognosis in this disease. Myocardial tomography, in particular, provided a more accurate evaluation of myocardial damage. Ventricular arrhythmias seem to be a serious problem in these patients. Therefore, careful observation using these tests, especially myocardial tomography and Holter monitoring, should be done even if the patients are free of symptoms.

Adolescent↗
PubMed1989

Molecular mimicry between uveitopathogenic site of retinal S-antigen and Escherichia coli protein: induction of experimental autoimmune uveitis and lymphocyte cross-reaction.

Experimental autoimmune uveitis (EAU) is caused by the immunization of microgram amounts of a soluble retinal protein, known as S-antigen, in susceptible animal strains including primates. The disease serves as an animal model of ocular inflammation. We induced EAU and pinealitis in Lewis rats with small synthetic peptides, corresponding to the amino acid sequence in Escherichia coli protein, which contains six consecutive amino acids identical to a uveitopathogenic site in human S-antigen (peptide M). EAU and pinealitis induced in rats by synthetic peptide derived from E. coli was indistinguishable from those induced by native S-antigen or other uveitopathogenic synthetic peptides corresponding to the amino acid sequence of S-antigen. Furthermore, lymph node cells from animals immunized with either peptide M or peptide derived from E. coli protein showed significant proliferation in the presence of either peptide when tested in vitro for lymphocyte mitogenesis using [3H]thymidine. Thus, molecular mimicry, a process by which an immune response directed against a nonself protein cross-reacts with a normal host protein, may play a role in autoimmunity.

Amino Acid Sequence↗
PubMed1989

Sequence homology between yeast histone H3 and uveitopathogenic site of S-antigen: lymphocyte cross-reaction and adoptive transfer of the disease.

Experimental autoimmune uveitis (EAU) serves as an animal model of ocular inflammation. The disease is caused by the immunization of microgram amounts of a soluble retinal protein, designated S-antigen, in susceptible animal strains, including primates. We induced EAU and experimental autoimmune pinealitis (EAP) in Lewis rats with a small synthetic peptide corresponding to amino acid positions 106-121 in yeast histone H3. This peptide contains five consecutive amino acids identical to a uveitopathogenic site (peptide M) in human S-antigen. Lymph node or mononuclear cells from different species of animals immunized either with histone H3 or with peptide M showed significant cross-reaction as measured by in vitro lymphocyte mitogenesis assay using [3H]thymidine. Also, we adoptively transferred the EAU and EAP in naive rats by immune lymph node cells. These findings support the fact that selected bacterial, viral, or fungal proteins with amino acid sequence homologies to normal retinal proteins are uveitopathogenic and, as such, provide a basis for autoimmune inflammatory diseases.

Amino Acid Sequence↗
PubMed1989

Host range bias of the JC virus mutant enhancer with DNA rearrangement.

JC-HEK, a JC virus (JCV) host range mutant adapted to growth in human embryonic kidney cells (HEK), has DNA rearrangement in the control region for early transcription. The 822-bp rearranged segment of JC-HEK (containing one authentic promoter-enhancer unit of 98 bp and truncated coding region of T-antigen and VP-1 genes) was inserted into pSV0cat vector and examined for expression of chloramphenicol acetyltransferase (CAT). The CAT activity induced by the mutant was comparable to that by the SV40 promoter-enhancer (pSV2cat) and four times as high as that by the prototype JCV (Mad-1) in HEK cells, whereas the two JCV promoter-enhancers were equally efficient in a permissive neuroblastoma cell line. On the other hand, both JC-HEK DNA with three DNA replication origins and Mad-1 DNAs replicated after transfection into HEK cells at a similar efficiency in the presence of JCV T-antigen. The elevated promotor-enhancer activity caused by the DNA rearrangement seems to play a major role in adaptation of JCV to growth in HEK cells.

Antigens, Polyomavirus Transforming↗
PubMed1989

The gene for retinal S-antigen (48-kDa protein) maps to the centromeric portion of mouse chromosome 1 near Idh-1.

S-antigen (48-kDa protein) is a soluble protein of the retina and the pineal gland that is believed to play an important role in the visual process. S-antigen is involved in the regulation of the activity of rod photoreceptor-specific cGMP-phosphodiesterase (cGMP-PDE). The activity of this enzyme has been shown to be deficient in the retina of the rd mouse, which is affected by an autosomal recessive disease characterized by degeneration of the photoreceptor cells. The abnormal cGMP-PDE activity could result from, among other things, a lesion in the enzyme itself or in any of the proteins that regulate it, such as the S-antigen. We have used a mouse cDNA clone for the S-antigen to map the corresponding gene, Sag, to mouse chromosome 1 near Idh-1. Since the rd gene is located on mouse chromosome 5, our results suggest that Sag is not the site of the rd mutation.

Animals↗
PubMed1989

Enhanced erythrocyte aggregability in occlusive cerebrovascular disease.

We measured the rate of erythrocyte aggregation using our whole-blood aggregometer in 80 patients with occlusive cerebrovascular disease during the acute and chronic phases. We compared the data with values for 38 age-matched healthy controls. Mean +/- SD erythrocyte aggregability of the patients during both the acute phase (0.145 +/- 0.21/sec, n = 35) and the chronic phase (0.139 +/- 0.21/sec, n = 45) was higher than that in the controls (0.123 +/- 0.21/sec, n = 38; p less than 0.01). Erythrocyte aggregability was positively correlated with the plasma concentration of globulin and fibrinogen and inversely correlated with the albumin:globulin ratio. However, these correlations did not necessarily exclude the possibility that some unknown substance(s) released from ischemic tissue might enhance erythrocyte aggregability.

Acute Disease↗
PubMed1989

[Continual observation of the blood vessels beneath the oral sulcular epithelium in man by means of periomicroscope. Morphological analysis during experimental gingivitis].

It is important to clarify the relationship between prosthetic appliances and periodontal tissues for ideal prosthetic restorations. And therefore objective methods which give proper diagnosis for the first stage of gingivitis are indispensable. The purpose of this study was to investigate, using Periomicroscope, alterations of the blood vessels beneath the oral sulcular epithelium during a human experimental gingivitis, and to establish relationship between observation by Periomicroscope and clinical and histologic findings on the first stage of gingivitis. The subjects were 22 student volunteers ages 20-29 years with clinically normal periodontal tissues. At upper anterior teeth, gingivitis was produced by withdrawing tooth brushing for 21 days. After 21 days clinically nearly moderate gingivitis and histopathologically nearly moderate chronic gingivitis were observed, while significant differences were obtained in the changing of the capillary loop form. From the results obtained by Periomicroscope, it was suggested that the continual observation by Periomicroscope was effective for the diagnosis of gingivitis.

Adult↗
PubMed1989

Uveitopathogenic sites in bovine S-antigen.

Experimental autoimmune uveitis (EAU) was observed in Hartley guinea pigs following immunization with high doses (200 micrograms) of four synthetic peptides designated peptide 3, K, N and M which correspond to amino acid positions 221-240, 241-260, 281-302, and 303 to 320 respectively in bovine S-antigen. Histopathologically, a moderate inflammatory response involving the uveal tract and retina was observed using peptide N and peptide M as immunogens, whereas peptide 3 and peptide K caused only a mild inflammatory response with very few inflammatory cells in the retina. In contrast, animals with EAU showed an associated pinealitis (EAP) characterized by an extensive lymphocytic infiltration of the central and subcapsular areas of the pineal gland. Lymph node cells of guinea pigs immunized with peptide 3, peptide K, peptide N or peptide M showed strong in vitro proliferative responses against the respective immunizing peptide as measured by [3H] thymidine uptake. The results suggest that under appropriate experimental conditions S-antigen may contain multiple pathogenic sites. The relevance of these studies in the pathogenesis of EAU is discussed.

Amino Acid Sequence↗
PubMed1989

An 18-mer peptide derived from the retinal S antigen induces uveitis and pinealitis in primates.

S-antigen, a photoreceptor cell protein, induces a predominantly T-cell mediated autoimmune uveitis in many vertebrate animals, including primates. Because of this activity and the finding of immune responses to S antigen in patients with uveitis, this protein has been implicated in the pathogenesis of uveitis in humans. Peptide M, an 18-amino acid component of S antigen, has previously been shown to be highly uveitopathogenic in rats and guinea pigs. We report here that peptide M is immunopathogenic in some monkeys, producing inflammatory changes in eyes and pineal glands similar to those induced by native S antigen. Monkeys with disease also developed intense immune responses to peptide M, measured by the lymphocyte proliferation assay. In addition, lymphocytes from these monkeys reacted against whole S antigen. Furthermore, lymphocytes from certain monkeys immunized with whole S antigen responded well against peptide M, thus indicating that this peptide is an immunodominant epitope in these animals. Two of the four monkeys immunized with peptide M did not develop disease. Lymphocytes from these two animals did not respond in culture against the peptide. Following immunization with the whole protein, these monkeys were capable, however, of developing cellular immunity against S antigen and one of them developed disease. The possible involvement of peptide M in the pathogenesis of uveitis in humans is discussed.

Animals↗
PubMed1989

Chromosome pattern in juvenile chronic myelogenous leukemia, myelodysplastic syndrome, and acute leukemia associated with neurofibromatosis.

We studied chromosomes of BM cells from four neurofibromatosis (NF) patients with leukemia. One patient had a normal diploid karyotype in the chronic phase of juvenile chronic myelogenous leukemia (JCML). When the the leukemia evolved into the accelerated phase, she had cells with 46,XX,-7,+der(7)t(3;7)(q21;p22); the abnormalities resulted in a partial 7p deletion. In another patient with JCML, BM cells in the accelerated phase had 45,XY,-7. The abnormal cells with monosomy 7 disappeared from the BM after chemotherapy but reappeared later in the course. Another patient developed refractory anemia with excess of blasts in transformation (RAEB-T) and had cells with 46,XX,-6,+r(6)(p23?q21?); the abnormalities resulted in partial 6p and 6q deletions. The other patient with ANLL had cells with 45,XX,-7. Our findings and review of data on nine other patients suggest that BM cells of NF patients with JCML in chronic phase have no microscopically detectable chromosome changes and that cells with chromosomal deletion emerge when JCML evolve into the accelerated or blast phase. Thus, deletion of the whole or part of certain chromosomes, such as chromosomes 6, 7, etc., may be an important step towards the evolution of JCML cells or the development of de novo acute leukemias in NF patients.

Child↗
PubMed1989

[Philadelphia-positive acute mixed leukemia with monosomy 7].

A 26-year-old male was admitted to our hospital because of fever and leukocytosis. On admission, a white blood cell count was 28,300/microliters with 46.5% blast cells and 16.0% atypical monocytoid cells, a hemoglobin level 13.7 g/dl, and a platelet count 15.0 X 10(4)/microliters. Bone marrow contained 58.8% of peroxidase-negative blast cells. He was diagnosed as acute lymphoblastic leukemia (ALL L2) according to the FAB classification. Chromosome analysis revealed the marrow cells to contain 45, XY, -7, t(9; 22) (q34; q11). On surface marker analysis, the leukemic cells were positive for both lymphoid (CD10) and myeloid markers (CD13). Two color flow-cytometric analysis showed two distinct populations with CD10 and CD1 3, respectively. Rearrangements of both immunoglobulin heavy chain and T cell receptor beta-chain were observed. The "breakpoint cluster region" on chromosome 22 was not rearranged. On the basis of these findings, we thought this case being acute mixed leukemia. He was refractory to AdVP therapy and BHAC-DMP therapy. He is now under treatment with A-Triple-V therapy.

Adult↗
PubMed1989

[Quantitative assessment of pulmonary regurgitation by two-dimensional Doppler color flow imaging: postoperative evaluation of patients with tetralogy of Fallot].

Pulmonary regurgitation (PR) is a serious event following surgical repair for tetralogy of Fallot. For quantitative assessments of PR using noninvasive methods, we performed Doppler color flow imaging in 38 children, whose ages ranged from three to 15 years. All images were obtained from one to 10 years after surgery. The right ventricle and pulmonary valve were demonstrated in the parasternal short-axis view. The images of PR flow were in red and were frozen when the area of a signal was maximum (early to mid diastole). The PR distance index (PRDI), which is the maximum PR flow distance divided by square root of the body surface area, was measured. The PR area index (the maximum PR flow area/body surface area) (PRAI) was also calculated using a track ball. Cardiac catheterization was performed for 12 patients without residual L-R shunts or any apparent tricuspid regurgitation. PR was graded (0 = absent, 1 = trivial, 2 = mild, 3 = moderate, 4 = severe) according to the projection of contrast medium in the right ventricle as seen on the main pulmonary arteriogram. The size of the right ventricle was expressed as the right ventricular end-diastolic volume (RVEDV; % of normal), as determined from the cineangiogram, and the tricuspid valve annulus diameter (TVD; % of normal) from a four-chamber view of the two-dimensional echocardiogram. There were significant differences between the PRDI and the PRAI of five patients with PR of grades 1-2 and those of seven patients with PR of grade 3-4 (p less than 0.01, p less than 0.01, respectively). There was significant correlation between the % RVEDV and the % TVD observed (r = 0.82, p less than 0.01). Significant negative correlations were observed between the PRDI and right ventricular ejection fraction (RVEF), and the PRAI and RVEF (r = -0.68, p less than 0.02; r = -0.82, p less than 0.01, respectively). RVEF was below normal in all seven patients (100%) with PR of grade 3 or more and in one of five patients (20%) with PR of grade 2 or less. The PRDI of 2.5 or more, or the PRAI of 4.0 or more was equivalent to a PR of grade 3 or more and was a reliable index of significant PR.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1989

[Two cases of B-cell lymphoma occurring in a mother and her daughter at the same time].

Many cases of familial aggregation of lymphoproliferative malignancy have been reported. But familial aggregation of non-Hodgkin lymphoma is less frequent than Hodgkin's disease, Burkitt's lymphoma, and adult T-cell leukemia. Here we report familial B-cell lymphomas occurring in a mother and her daughter at the same time. The daughter (43 years old) was admitted because of fever. She died of a rapidly progressive neurological disturbance. The mother (75 years old) was admitted because of fever and pleural effusion, and then died with a complication of cryoglobulinemia. The histological findings of their lymph nodes revealed diffuse lymphoma, medium-sized cell type, with B-cell phenotype and mixture of cleaved and non-cleaved nuclei. They had no common chromosome abnormalities, while they shared HLA-A 2, B 35, and Cw 3 antigen. Viral infection was not identified, by routine serological test and electronmicroscopic study.

Adult↗