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Biomedical subjects

S Ando

Publications and source records attributed to S Ando.

At least 307 records · Page 17Linked to original sources

Use of a buccal musculomucosal flap to close palatal fistulae after cleft palate repair.

Forty-two patients aged 4 to 13 (mean 7 years) had palatal fistulae closed with a buccal musculomucosal flap. The pedicle was divided approximately 2 weeks after the initial operation. Complete closure at the first attempt was obtained in 69% of the cases though, when the fistulae were large and extended to the anterior hard palate, the results were not as good (36%). Almost no detrimental after-effects occurred at the donor site. The buccal musculomucosal flap was found to be a useful alternative to a tongue flap.

Adolescent↗

HLA-DP+ T cells and deficient interleukin-2 production in patients with systemic lupus erythematosus.

In patients with systemic lupus erythematosus (SLE), frequency of the T cells positive for HLA-DP, one of the major histocompatibility complex (MHC) class II molecules, was markedly increased in peripheral blood lymphocytes (PBL), in association with an increase in the amount of specific cytoplasmic transcript of the HLA-DP gene segment. Cell cycle analysis showed that HLA-DP is an early activation marker of T cells and that the high ratios of HLA-DP+ T cells from SLE patients are associated with high frequency of T cells at early activation phases, mainly of G1A. Initial high ratios of HLA-DP+ T cells decreased to a great extent during 4 days of in vitro culture, in the absence of mitogens. This event was associated with decreases in the amount of HLA-DP transcript and the disappearance of activated T cells. Studies on the interleukin 2 (IL-2) production of T cells from patients with SLE demonstrated that while the PBL rich in HLA-DP+ T cells show a markedly low production of IL-2, preculture of these PBL restores the ability to produce IL-2. Thus, it appears that the T cells in patients with SLE are essentially intact with regard to the capacity to produce IL-2 and that T cell activation events continuously occurring in SLE patients are related to a deficiency in IL-2 production. The possible underlying mechanisms are discussed.

Adolescent↗

Age-independent forearm vasodilatation by acetylcholine and adenosine 5'-triphosphate in humans.

1. Forearm vasodilator responses to acetylcholine, ATP and sodium nitroprusside were examined in healthy young (20 +/- 1 years, n = 9), middle-aged (46 +/- 2 years, n = 6) and old (57 +/- 1 years, n = 6) subjects. 2. A brachial artery was cannulated with a 20-gauge cannula through which drugs at graded doses were locally infused for 2 min at each dose. During drug infusions, forearm blood flow was continuously measured at 15 s intervals using a plethysmograph. Forearm vascular resistance was calculated from forearm blood flow and mean blood pressure obtained in the opposite arm. Basal forearm blood flow and forearm vascular resistance did not differ between the three groups. 3. Acetylcholine and ATP were used to examine endothelium-dependent vasodilatation, and sodium nitroprusside was used to examine endothelium-independent vasodilatation. All three drugs caused dose-dependent increases in forearm blood flow (P less than 0.01) and decreases in forearm vascular resistance (P less than 0.01). The increases in forearm blood flow or decreases in forearm vascular resistance in response to infusions of the three drugs did not differ between the three groups. 4. These results suggest that endothelium-dependent and endothelium-independent vasodilatation in forearm resistance arteries do not alter with ageing in humans.

Acetylcholine↗

Effects of cytokines from virus-induced human lymphoblasts on the growth and viability of the promyelocytic leukemia cell line HL-60.

Cells of the human B-cell lymphoblastic leukemia line, BALL-1, were stimulated with Sendai virus. It is shown that the crude culture supernatants contain not only interferon-alpha (IFN-alpha) and tumor necrosis factor-alpha (TNF-alpha) but also other cytokines, here collectively termed 'X' cytokines. The latter did not affect the cytostatic or differentiation-inducing effect of IFN-alpha but synergistically increased the cytotoxicity of TNF-alpha.

Burkitt Lymphoma↗

Effects of prolonged exposure to interferon-alpha on the viability, proliferation, differentiation, and tumorigenicity of HL-60 promyelocytic leukemia cells.

HL-60 promyelocytic leukemia cells were cultured continuously in the presence of 22,000 IU/ml of purified interferon-alpha (IFN-alpha) for up to 469 days. Study of the properties of the cells at various times during this period showed some changes in their expression of IgG Fc receptors, and in the maturation of the cells as indicated by their esterase content. The differences from control cells cultured in parallel were most marked after exposure to IFN-alpha for some 40-300 days, but were no longer seen after 400-470 days. The difference in tumorigenicity was significant after 150 days, but no longer after 300 days.

Animals↗

Identification of the second major allergen of Japanese cedar pollen.

We isolated and characterized the second major allergen (Cry j II) from Japanese cedar pollen. We found that most patients with this pollinosis had IgE antibody to this protein in addition to IgE antibody to Cry j I; however, some sera reacted only with Cry j I or Cry j II. IgE-ELISA inhibition studies revealed that Cry j I and Cry j II had no cross-allergenicity. Cry j II did not react with anti-Cry j I monoclonal antibodies. In SDS-PAGE under a non-reducing condition, Cry j II showed a band at the 37 kDa position, compared with the 45-50 kDa bands of Cry j I. N-terminal amino acid sequence of Cry j II was completely different from that of Cry j I.

Allergens↗

Synaptic membrane aging in the central nervous system.

Membrane potentials involved in neuronal excitability, transmitter uptake and so on were determined using synaptosomes from different age groups of mice. Synaptosomal resting membrane potential was found to decrease significantly in senescence. Concomitantly decreased activity of an electrogenic enzyme, Na+,K(+)-ATPase, was interpreted by two mechanisms. In senescence, the decreased content of phosphatidylcholine seemed responsible in part for decreased enzyme activity due to the modified lipid microenvironment. In the late stages of senescence, decreased enzyme content may rather cause reduction of enzyme activity, leading to a less negative set point of the membrane potential.

Aging↗

Attenuated forearm vasodilative response to intra-arterial atrial natriuretic peptide in patients with heart failure.

It has been shown that renal responses to atrial natriuretic peptide (ANP) are markedly attenuated in patients with heart failure. This study aimed to determine if vasodilative response to ANP is altered in patients with heart failure. In patients with heart failure (n = 7) and age-matched normal subjects (n = 7), forearm blood flow was measured using a strain-gauge plethysmograph during intra-arterial infusion of alpha-human ANP (50, 100, 200, and 400 ng/min) or nitroglycerin (100, 200, 400, and 600 ng/min). Forearm vasodilatation evoked with intra-arterial alpha-human ANP in patients with heart failure was considerably less (p less than 0.01) than that in normal subjects. In contrast, nitroglycerin produced comparable forearm vasodilatation in the two groups. Plasma ANP and cyclic guanosine monophosphate (GMP) levels at rest were higher in patients with heart failure than in normal subjects (p less than 0.05 for both), but the increases in plasma ANP and cyclic GMP in the venous effluents during intra-arterial ANP infusion did not differ between the two groups. These results indicate that the direct vasodilative effect of ANP on forearm vessels was attenuated in patients with heart failure as compared with that in normal subjects. The mechanisms responsible for this alteration are not clear but might involve mechanisms other than down-regulation of the ANP receptors because the increases in venous plasma cyclic GMP caused by intra-arterial ANP were comparable between patients with heart failure and normal subjects.

Adult↗

Pathology of experimental chlamydiosis in chicks.

Twelve one-day-old chicks were experimentally inoculated with Chlamydia psittaci derived from turkeys. Acute chlamydial septicemic lesions were induced by the inoculation into the air sac and trachea. No lesions were produced by the esophageal injection. Clinically, the affected chicks showed emaciation and mouth breathing, and were inactive while some birds died. Grossly, they had hepatomegaly, splenomegaly and airsacculitis. Histopathologically, fibrinopurulent airsacculitis, pneumonia and bronchitis, multiple fibrinous serositis in the hepatic and splenic capsules, peri- and epicardium, and mesenterium, focal endoarteritis in the aortae, activation of reticuloendothelial cells in the spleen, and hepatic necrosis were noted. Immunohistochemically, chlamydial antigen granules were present in the cytoplasm of epithelial cells of the respiratory system, hepatocytes, macrophages in the air sac, lung, serous membrane, liver, spleen, aortae, reticuloendothelial cells in the spleen, and mesothelial cells in various organs or tissues. Chlamydial multiplication in the cells of the organs or tissues involved was preceded to form the lesions.

Air Sacs↗

Biological and immunological properties of Sugi basic protein-pullulan conjugate. II. Is the reduced ability to elicit the Arthus reaction based on the poor activation of complement by immune complex consisting of anti-Sugi basic protein and Sugi basic protein-pullulan?

Ability of Sugi basic protein (SBP)-pullulan conjugate to elicit the Arthus reaction was found to be markedly reduced, about 100 times lower than that of native SBP. To analyze this reduced ability, activation of complement by immune complex consisting of SBP-pullulan and anti-SBP antibodies was studied. Tests for complement consumption, C3 conversion and cleavage of factor B revealed that immune complex formed with SBP-pullulan is incapable of supporting efficient activation of the complement system. Previously, we have shown data suggesting that SBP-pullulan conjugate would be a good candidate for desensitization therapy against cedar pollinosis. The results presented in this paper provide additional support for the suggestion.

Allergens↗

Structure of phosphonoglycosphingolipid containing pyruvylated galactose in nerve fibers of Aplysia kurodai.

A phosphonoglycosphingolipid, designated as FGL-IIb, was identified in nerve fibers of Aplysia kurodai by two-dimensional thin layer chromatography (Abe, S., Araki, S., and Satake, M. (1986) Biomed. Res. (Tokyo) 7, 47-51). FGL-IIb was isolated from the nervous system of A. kurodai by Iatrobeads column chromatography using three solvent systems. Pyruvic acid was identified by thin layer chromatography as its 2,4-dinitrophenylhydrazone and established by permethylation studies to be attached as a ketal to O-3 and O-4 of the terminal galactose of the oligosaccharide chain in FGL-IIb. By sugar analysis, permethylation studies, fast atom bombardment-mass spectrometry, and proton magnetic resonance spectrometry, the structure of FGL-IIb was concluded to be [3,4-O-(1-carboxyethylidene)]Gal beta 1----3GalNAc alpha 1----3(Fuc alpha 1----2) (2-aminoethylphosphonyl----6)Gal beta 1----4Glc beta 1----1ceramide. Its major aliphatic components were palmitic acid, octadeca-4-sphingenine and anteisononadeca-4-sphingenine. This is the first report of the occurrence of pyruvylated galactose as a constituent of animal sphingolipid.

Acidic Glycosphingolipids↗

Developmentally expressed O-acetyl ganglioside GT3 in fetal rat cerebral cortex.

Monoclonal antibody M6704, established against the chick neural tube, was shown to recognize a trisialosyl residue, NeuAc alpha 2-8NeuAc alpha 2-8NeuAc alpha 2-3-R of C-series gangliosides. Using this antibody, the developmental changes of C-series gangliosides in fetal rat cerebral cortex have been examined. Two dimensional thin layer chromatography (TLC) enzyme-immunostaining analysis revealed that alkali treatment resulted in a great increase in GT3 that amounted to more than 85% of the total GT3 detected. The alkalilabile form was easily degraded to form GT3 by the action of the receptor-destroying enzyme of influenza C virus, sialate O-acetylesterase, indicating that the antigen was most probably 9-O-acetyl-NeuAc containing GT3. The ganglioside was highly enriched at the 14th gestation day, gradually decreased, and was not detected in adult rat cerebral cortex.

Aging↗

Communicating hydrocephalus occurring in the postoperative course of glioblastoma multiforme.

We experienced a case of glioblastoma multiforme which exhibited dementia, gait disturbance, headache, and urinary incontinence six months after subtotal removal of the tumor. These symptoms were not due to tumor recurrence, but to communicating hydrocephalus. Communicating hydrocephalus in cases of malignant brain tumors has not often been reported. We discuss the development of this abnormality.

Brain Neoplasms↗

Protein kinase C phosphorylation of desmin at four serine residues within the non-alpha-helical head domain.

We reported that phosphorylation by either cAMP-dependent protein kinase or protein kinase C (Ca2+/phospholipid-dependent enzyme) in vitro induces disassembly of the desmin filaments (Inagaki, M., Gonda, Y., Matsuyama, M., Nishizawa, K., Nishi, Y., and Sato, C. (1988) J. Biol. Chem. 263, 5970-5978). For this subunit protein, Ser-29, Ser-35, and Ser-50 within the non-alpha-helical head domain were shown to be the sites of phosphorylation for cAMP-dependent protein kinase (Geisler, N., and Weber, K. (1988) EMBO J. 7, 15-20). In the present work, we identified the sites of desmin phosphorylated in vitro by other protein kinase which affects the filament structure. The protein kinase C-phosphorylated desmin was hydrolyzed with trypsin, and the phosphorylated peptides were isolated by reverse-phase chromatography. Sequential analysis of the purified phosphopeptides, together with the known primary sequence, revealed that Ser-12, Ser-29, Ser-38, and Ser-56 were phosphorylated by protein kinase C. All four sites are located within the non-alpha-helical head domain of desmin. Ser-12, Ser-38, and Ser-56, specifically phosphorylated by protein kinase C, have arginine residues at the carboxyl-terminal side (Arg-14, Arg-42, and Arg-59, respectively). Ser-29 phosphorylated by both protein kinase C and cAMP-dependent protein kinase has arginine residues at the amino and carboxyl termini (Arg-27 and Arg-33). These findings support the view that the head domain-specific phosphorylation strongly influences desmin filament structure; however, each protein kinase differed with regard to site recognition on this domain.

Amino Acid Sequence↗

Domain- and sequence-specific phosphorylation of vimentin induces disassembly of the filament structure.

We reported that stoichiometric phosphorylation by either cAMP-dependent protein kinase or protein kinase C induces disassembly of vimentin filaments [Inagaki, M., Nishi, Y., Nishizawa, K., Matsuyama, M., & Sato, C. (1987) Nature 328, 649-652; Inagaki, M., Gonda, Y., Matsuyama, M., Nishizawa, K., Nishi, Y., & Sato, C. (1988) J. Biol. Chem. 263, 5970-5978]. In the present work, we attempted to identify the sites of vimentin phosphorylated by each protein kinase. Sequential analysis of the purified phosphopeptides, together with the known primary sequence, revealed that Ser-8, Ser-9, Ser-20, Ser-25, Ser-33, and Ser-41 were specifically phosphorylated by protein kinase C, whereas Ser-46 was phosphorylated preferentially by cAMP-dependent protein kinase. Both kinases reacted with Ser-6, Ser-24, Ser-38, Ser-50, and Ser-65. Specific phosphorylation sites for protein kinase C are mostly located close to the amino-terminal side of arginine while those for cAMP-dependent protein kinase are located close to the carboxyl-terminal side of arginine. The phosphorylation sites exclusively occur in the amino-terminal non-alpha-helical head domain, particularly at the beta-turn region. These results provide clues to the molecular mechanisms of phosphorylation-dependent disassembly of vimentin filaments.

Amino Acid Sequence↗