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Biomedical subjects

N Ono

Publications and source records attributed to N Ono.

At least 19 recordsLinked to original sources
PubMed1992

Histogenesis of diffuse small cleaved cell lymphoma. An immunohistochemical and molecular genetic (bcl-2 gene) study with comparison to follicular small cleaved cell lymphoma and mantle zone lymphoma.

Immunohistochemical and molecular genetic (bcl-2 gene) studies were performed on specimens from 24 patients with follicular small cleaved cell lymphoma (FSCCL), 24 patients with diffuse small cleaved cell lymphoma (DSCCL) and 4 patients with mantle zone lymphoma (MZL) to determine the cellular origin of the disease and whether or not DSCCL represents the diffuse counterpart of FSCCL. Two patients with FSCCL, 22 patients with DSCCL, and all of the patients with MZL had a phenotype of mantle zone (MZ) B-lymphocytes (SIgD+, Leu-1+, Leu-8+, positive alkaline phosphatase [ALPase+], and negative common acute lymphoblastic leukemia antigen [CALLA-]), and all the tested patients (2 patients with FSCCL, 13 patients with DSCCL, and 4 patients with MZL) had germlines of bcl-2 gene. Fourteen patients with FSCCL and 1 patient with DSCCL had a phenotype of follicular center cells (FCC) (CALLA+, SIgD-, Leu-1-, Leu-8- and negative ALPase), and 11 patients with FSCCL had bcl-2 gene rearrangements. These results indicate that FSCCL are almost always derived from FCC, whereas some FSCCL, most DSCCL, and all MZL are derived from MZ B-lymphocytes, and these lymphomas should be included in the same category as MZ B-lymphocyte-derived lymphomas. Histologically diagnosed DSCCL often may represent a diffuse counterpart of MZ B-lymphocyte-derived lymphoma. MZ B-lymphocyte-derived lymphomas histologically show a follicular (nodular), a follicular MZ, or a diffuse growth pattern and clinically show a high incidence of peripheral blood (PB) involvement or bone marrow (BM) involvement.

Adult↗
PubMed1992

Serine residues responsible for tetracycline transport are on a vertical stripe including Asp-84 on one side of transmembrane helix 3 in transposon Tn10-encoded tetracycline/H+ antiporter of Escherichia coli.

Putative transmembrane helix 3 of the tetracycline/H+ antiporter encoded by a transposon, Tn10, contains four serine residues, Ser-77, Ser-82, Ser-91 and Ser-92. Each of these serine residues was replaced by site-directed mutagenesis. Of these four serine residues, Ser-77 was important for the transport function, and a bulky side chain at position 91 hindered substrate translocation, whereas Ser-82 and Ser-92 did not play any role. Ser-77 and Ser-91 are on the same vertical stripe, that includes the essential Asp-84, on the hydrophilic side of putative helix 3. These observations suggest that helix 3 is part of the tetracycline translocation channel across the membrane.

Alanine↗
PubMed1992

Metal-tetracycline/H+ antiporter of Escherichia coli encoded by transposon Tn10. Roles of the aspartyl residues located in the putative transmembrane helices.

Three conserved aspartyl residues located in the putative transmembrane helices in the Tn10-encoded metal-tetracycline/H+ antiporter were replaced by Asn, Lys, or Glu with oligonucleotide-directed site-specific mutagenesis. Replacement of Asp84 or Asp15 by Asn or Lys caused a severe defect in tetracycline transport activity, however, the Glu84 and Glu15 mutants retained 150 and 40% of the wild type activity, respectively, indicating the critical role of the negative charge. The increase in the activity of the Glu84 mutant was due to an increase in the affinity for the substrate. H+/tetracycline coupling was intact in these mutants, including Asn and Lys mutants. On the other hand, all of the Asp285-substitution mutants showed a severe defect in tetracycline transport activity and a complete lack of tetracycline-coupled H+ transport. However, since in vivo tests showed the tetracycline resistance for the Glu285 mutant, a negative charge in position 285 plays some role in maintaining the possible down-hill and/or low affinity efflux of accumulated tetracycline from intact cells. Similar work was done for Asp365, and here the Asn and Glu mutants showed decreased but high activity, while the Lys mutant was only marginally active (5%), indicating that a negative charge is not so demanding in position 365, possibly because it is not in the membrane.

Amino Acid Sequence↗
PubMed1992

Suprasellar germinomas; relationship between tumour size and diabetes insipidus.

The clinical and neuro-endocrinological aspects of 17 suprasellar germinoma patients treated between 1972-1991 are reported. Surgical extirpation was not initially attempted, but all patients received irradiation with or without a biopsy. Sixteen of those have led useful lives with appropriate hormonal replacement therapy during a mean follow up of 8 years. Seven tumours at diagnosis were less than 2 cm in diameter (type 1), nine tumours more than 2 cm (type 2), and one double midline tumour was of unknown size. All 7 type 1 patients required 1-deamino-8-D-arginine-vasopressin (DDAVP) to control diabetes insipidus (DI), but only 2 of the 9 type 2 patients have needed DDAVP since completion of the treatment. Patients with smaller tumours required more DDAVP following tumour disappearance, than those with larger tumours. The prognostic indicators for the post-treatment course of DI and retarded growth appeared to be the tumour size and the age at diagnosis. We also emphasize the absence of metastasis in unoperated cases and the use of tumour markers as a diagnostic criterion which obviates surgical acquisition of tissue to make the diagnosis. Possible reasons are discussed and the literature reviewed.

Adolescent↗
PubMed1992

Physiologic capacity of well-developed collaterals in patients with isolated left anterior descending artery disease.

To assess the physiologic significance of well-developed collaterals, 34 patients, with isolated left anterior descending artery disease (LAD) and without overt prior myocardial infarction, underwent cardiac catheterization and exercise thallium-201 emission computed tomography. The patients were divided into 3 groups; 11 patients with 90% stenosis of the proximal LAD and without collaterals (group 1), 11 with 99% stenosis of the proximal LAD, and without collaterals (group 2) and 12 with a total occlusion of the proximal LAD which was completely filled by well-developed collaterals (group 3). On left ventriculography, shortening fractions of the anterior wall were significantly reduced in group 2 as compared to group 1 and 3 (group 1 vs group 2: p less than 0.01, group 2 vs group 3: p less than 0.05), which reflected the lower ejection fraction of group 2 (p less than 0.01 and p less than 0.05, respectively). The perfusion defects of the anterior wall on both the initial and the delayed images were severer in groups 2 and 3 than in group 1 (group 1 vs group 2 and group 1 vs group 3 on the initial image: p less than 0.01, for both, group 1 vs group 2 and group 1 vs group 3 on the delayed image: p less than 0.05, for both). However, recovery of the perfusion defects from the initial image to the delayed image was better in group 3 than in groups 1 and 2 (group 1 vs group 2 and group 1 vs group 3: p less than 0.05, for both). Therefore, coronary blood flow through well-developed collaterals was considered to be comparable to the flow through a diseased vessel with 90% stenosis at rest. During maximal exercise, blood flow through well-developed collaterals was considered to be comparable to the flow through a diseased vessel with 99% stenosis, although the blood flow through well-developed collaterals was considered to be better than that through 99% stenosis during the recovery period. These findings suggest that patients with well-developed collaterals must be treated like those with severe stenosis.

Aged↗
PubMed1992

Circadian fluctuations of tissue plasminogen activator antigen and plasminogen activator inhibitor-1 antigens in vasospastic angina.

To elucidate the circadian variation of fibrinolytic components in vasospastic angina, plasma levels of tissue plasminogen activator antigen (t-PA), free plasminogen activator inhibitor antigen (free PAI-1), t-PA/PAI-1 complex, and total PAI-1 were measured in venous plasma samples. Samples were taken every 6 hours (6:00 AM, noon, 6:00 PM, and midnight) for 24 hours in 14 patients with vasospastic angina, in 9 patients with exertional angina, and in 19 normal subjects. Twenty-four-hour Holter monitoring (Holter monitor, Del Mar Avionics, Irvine, Calif.) was also carried out in all subjects. All of the fibrinolytic components showed circadian variation, with a peak level at 6:00 AM in every study group except for the t-PA/PAI-1 complex in the group of patients with exertional angina. The values for all or the fibrinolytic components at each sampling time were higher in patients with coronary artery disease than in normal subjects. In particular, the mean value of free PAI-1 at 6:00 AM in patients with vasospastic angina was significantly higher than that in normal subjects and that in patients with exertional angina. This value of free PAI-1 in patients with vasospastic angina was closely associated with the duration of ischemic attacks. These results suggested that the circadian fluctuation of fibrinolytic components may be an important factor that leads to coronary thrombosis at the time of coronary spasm, especially in the early morning.

Acetylcholine↗
PubMed1992

Influences of cyclooxygenase inhibitors on the cataleptic behavior induced by haloperidol in mice.

Haloperidol administered intraperitoneally, and prostaglandin F2 alpha (PGF2 alpha) and PGE2 intraventricularly induced dose-dependent cataleptic behavior in mice. The cataleptic behavior induced by haloperidol was inhibited dose-dependently by oral pretreatment with aspirin and indomethacin, inhibitors of PGs synthetase. Striatal 3,4-dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindole 3 acetic acid (5-HIAA) were elevated by haloperidol, although dopamine (DA) and 5-hydroxytryptamine (5-HT) levels did not change. The increase of DOPAC level in striatum induced by haloperidol was significantly suppressed by aspirin, but not in brain stem. The alteration of DOPAC level by aspirin correlated with the behavioral response. These results suggest that central prostaglandin synthesis may participate in the development of cataleptic behavior, which might also involve alteration of brain catecholaminergic activity.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1992

A familial case of hyper-IgM immunodeficiency.

A 22-year-old male was diagnosed as having immunodeficiency with hyper-IgM based upon recurrent pneumonia, marked elevation of serum IgM and markedly decreased level of IgG. IgG-or IgA-bearing B cells were not detected in peripheral blood while a number and a proportion of peripheral blood T lymphocytes were normal. Peripheral blood lymphocytes from this patient proliferated normally in response to T-independent and T-dependent B cell mitogens, and to T cell mitogens. Furthermore, the same type of dysgammaglobulinemia with increased IgM was found in the patient's father and brother. From these observations, it is suggested that it is a rare case of autosomal dominant or polygenal inheritance of hyper-IgM immunodeficiency.

Adult↗
PubMed1992

Two fatal cases of hepatitis B virus carriers after corticosteroid therapy for bronchial asthma.

We report two hepatitis B virus (HBV) carriers who had liver failure after withdrawal of corticosteroids (steroids) administered for treatment of serious asthmatic attacks. Liver functions deteriorated 1 to 2 wk after withdrawal of the steroid therapy and liver failure occurred. Steroid readministration and intensive therapy for liver failure did not prevent death. An excessive immune response provoked by steroid withdrawal and decreased reserve capacity due to underlying chronic liver disease were thought to be factors in the liver failure. Caution must be exercised in the administration of steroids to patients with underlying chronic HBV infection to prevent exacerbation of hepatitis. Prompt readministration of steroids is indicated if evidence of liver failure develops.

Aged↗
PubMed1992

Lysinuric protein intolerance presenting deficiency of argininosuccinate synthetase.

A 35-yr-old woman, who suffered from relapsing coma with hyperammonemia for 17 yr, was diagnosed to have lysinuric protein intolerance (LPI). Increased urinary dibasic amino acids (lysine, arginine and ornithine) and impaired absorption of orally administered lysine and arginine proved the defects of renal tubular and intestinal transport of dibasic amino acids. These defects are the primary cause of impaired urea cycle metabolism in LPI. Further, the level of argininosuccinate synthetase (ASS), a urea cycle enzyme, was analyzed and it was found to be below the normal level. This is the second reported case of LPI presenting ASS deficiency.

Adult↗
PubMed1992

[Intra-arterial infusion chemotherapy for hepatocellular carcinoma using an implantable drug delivery system].

Intra-arterial chemotherapy and chemoembolization using implantable drug delivery system were performed in sixty-one cases of unresectable hepatocellular carcinoma (HCC). The following results were obtained. (1) The follow-up period was 253 days, and the administrations numbered 13.9 times on average. (2) Response rate was 31.1%. (3) AFP decreased in 80% cases, and PIVKA-II in 83.3% cases. (4) Tumor thrombus in the portal vein disappeared in 4 of 40 cases(10%). (5) Free-CDDP continued for 60 minutes after injection of cisplatin-phosphatidyl-choline-Lipiodol (CPL), and the response rate was 47%. (6) The survival rates were 56% in one year, 25% in two years, and 20% for three years. These results were significantly higher than those of one shot therapy. It is suggested that good therapeutic effects can be obtained by the implantable drug delivery system, and CPL was a useful anticancer agent for the therapy.

Biomarkers↗
PubMed1992

[A case of congenital long QT syndrome associated with T wave alternans].

A case was presented in which a rare T wave alternans occurred in association with congenital long QT syndrome. A 71-year-old woman, who had experienced several syncopal attacks per year for the previous forty years, was admitted for further evaluation of the syncope. She had a family history of sudden death (sister) and QT prolongation (son). Electrocardiogram showed a corrected QT interval of 0.68 seconds. Treadmill exercise-tolerance test revealed both T wave alternans immediately after exercise and torsades de pointes 150 seconds after exercise. The syncope was induced by the mental excitation. A prolonged corrected QT interval reduced from 0.70 seconds to 0.58 seconds by the correction of her serum potassium and magnesium. The effect of propranolol, verapamil, phenytoin or mexiletine on T wave alternans and ventricular arrhythmia was evaluated by the treadmill exercise-tolerance test. The treatment with propranolol was most effective.

Adrenergic beta-Antagonists↗
PubMed1992

[Exercise-induced left bundle branch block in treadmill exercise test: clinical significance and prognosis].

Exercise induced left bundle branch block (LBBB) is poorly understood. We investigated its clinical characteristics and prognosis. The records of 3,459 consecutive patients who underwent treadmill exercise testing were reviewed. Exercise induced LBBB was identified in 6 patients (0.17%). Three out of six patients had underlying cardiac disease; two had coronary artery disease and one dilated cardiomyopathy. Three out of five had redistribution on Tl-201 myocardial scintigraphy. In one of these three patients, however, coronary angiography demonstrated no significant narrowings. Tl-201 myocardial scintigraphy in patients with exercise induced LBBB may be undetermined for coronary artery disease. During follow-up, one of six patients had depressed left ventricular function and was diagnosed as having dilated cardiomyopathy. It is thus obvious that exercise induced LBBB without a specific underlying heart disease should be followed up carefully.

Aged↗
PubMed1992

[CD3-negative natural killer cell leukemia with aggressive clinical course].

The authors report an autopsy case of CD3- large granular cell leukemia with an aggressive clinical course. A 15-year-old male was admitted to our hospital with complaint of high fever. Clinical examination revealed cervical lymphadenopathy and hepatosplenomegaly. His white blood cell count was 7,000/microliters with 45% large granular lymphocytes. A biopsy specimen of the cervical lymph node showed diffuse lymphoma, mixed small and large cells (DM). Surface marker analysis by immunohistochemical technique revealed that neoplastic cells expressed CD2, CD38, CD56 and HLA-DR but lacked CD3, CD4 and CD8. Southern blot analysis of immunoglobulin (Ig) and T cell receptor (TCR) genes showed germ line of Ig and TCR. These findings indicate that this case was a large granular cell leukemia with the natural killer cell phenotype. Despite anti-leukemic therapy, he died of hyperkalemia and acidosis. Autopsy showed a marked swelling of the liver (3,122 g) and spleen (2,434 g) with leukemic cell infiltration.

Adolescent↗
PubMed1991

Stoichiometry of metal-tetracycline/H+ antiport mediated by transposon Tn10-encoded tetracycline resistance protein in Escherichia coli.

The tetracycline resistance protein (TetA) endoded by transposon Tn10 mediates the efflux of divalent cation-tetracycline chelating complexes [Yamaguchi, A., Udagawa, T. and Sawai, T. (1990) J. Biol. Chem. 265, 4809-4813]. It was confirmed that protons were antiported with the complexes through an electrically-neutral process because the antiport consumed delta pH but not delta psi. The quantitative relationship between delta pH and delta pTC determined by a flow-dialysis method clearly indicated a 1:1 stoichiometry of the monocationic metal-tetracycline/H+ exchange.

Cell-Free System↗
PubMed1991

Metal-tetracycline/H+ antiporter of Escherichia coli encoded by a transposon Tn10. Histidine 257 plays an essential role in H+ translocation.

The transposon Tn10-encoded tetA gene product is a metal-tetracycline/proton antiporter (Yamaguchi, A., Udagawa, T., and Sawai, T. (1990) J. Biol. Chem. 265, 4809-4813). Its tetracycline transport activity was inhibited by a histidine-specific reagent, diethyl pyrocarbonate. Among five histidine residues in this antiporter, only His257 is located in the putative transmembrane helices. Thus, His257 was replaced by Glu or Asp. Inverted vesicles containing the Glu257 and Asp257 mutant proteins showed only 20 and 10% of the tetracycline uptake of wild-type vesicles, respectively. In contrast to wild-type vesicles, the mutant vesicles showed no tetracycline-dependent proton translocation, indicating that the mutant proteins had lost the tetracycline/H+ antiport activity. The significant 60Co2+ uptake without proton translocation by the mutant vesicles also confirmed that the mutant carriers act as uniporters of a metal-tetracycline complex. The metal-tetracycline uniport by the mutant proteins was not inhibited by diethyl pyrocarbonate, indicating that His257 is the only histidine residue essential for proton translocation. These mutant proteins conferred about half-level resistance to tetracycline, probably due to their catalyzing downhill efflux of a metal-tetracycline complex out of the cells.

Amino Acid Sequence↗
PubMed1991

Generation and characterization of the human immunodeficiency virus type 1 mutants.

Mutations were introduced by recombinant DNA techniques into 9 genes of an infectious molecular clone of human immunodeficiency virus type 1. The 24 mutants generated were characterized biochemically and biologically by transfection and infection experiments. None of the mutants which have mutations in gag (p17, p24, and p15 regions), pol (protease, reverse transcriptase, and endonuclease domains), env (gp120 region), tat, or rev were infectious, whereas vif, vpr, vpu, some of env (gp41) and nef mutants could grow in human CD4+ cells to various degrees. Of the non-infectious mutants, only endonuclease (pol) and gp41 mutants exhibited normal phenotypes with respect to the production of functional reverse transcriptase, the expression of gag, pol, and env proteins, and the generation of progeny virions, when examined in transient assays. All infectious mutants killed the CD4+ cells with the exception of a mutant carrying a defect in the vif gene.

Blotting, Western↗