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Biomedical subjects

H Mikawa

Publications and source records attributed to H Mikawa.

At least 181 records · Page 10Linked to original sources
PubMed1989

[Successful induction chemotherapy for childhood RAEB-T with VP-16: a case report].

A one-year-old boy diagnosed as refractory anemia with excess of blasts in transformation is reported. Hematological examination revealed anemia, thrombocytopenia and the presence of blasts in both peripheral blood (3.5%) and bone marrow (20.1%) specimens. Chromosomal analysis showed abnormal karyotype; 48, XY, +21, +marker, r (7). Analyses with cytochemical stainings, electronmicroscopy and monoclonal antibodies to cell surface markers could not define the lineage of blasts. Induction chemotherapy was started with VP-16 (230 mg/m2 x 5 days) as a single agent and complete remission was achieved. Thereafter, he had been treated for 11 months with the intensive chemotherapy which consisted of VP-16, cytosine arabinoside, daunorubicin, vincristine, vinblastine, 6-mercaptopurine, prednisolone, mitoxantrone and CNS prophylaxis. He has been in complete remission for 18 months. The usefulness of VP-16 to MDS in pediatric patients is documented.

Anemia, Refractory, with Excess of Blasts↗
PubMed1988

Regulation of Fc epsilon R2/CD23 gene expression by cytokines and specific ligands (IgE and anti-Fc epsilon R2 monoclonal antibody). Variable regulation depending on the cell types.

The regulation of human low affinity FcR for IgE (Fc epsilon R2/CD23) and the soluble Fc epsilon R2 [IgE binding factor (BF)] of monocyte (U937), T (ED), and B (JIJOYE) cell lines was examined by anti-Fc epsilon R2 mAb (H107, Mab176) and the cDNA probe for Fc epsilon R2. The effect of IL-4 and IFN-gamma on Fc epsilon R2 regulation was variable among these three cell lines. IL-4 and IFN-gamma enhanced the Fc epsilon R2 gene expression and the production of Fc epsilon R2 and IgE-BF on U937, whereas IL-4 and IFN-gamma had no significant effect on the Fc epsilon R2 expression on ED. On JIJOYE, IL-4 enhanced the Fc epsilon R2 and IgE-BF production on both protein and mRNA levels. In U937 and JIJOYE cells, there was a marked increase of Fc epsilon R2 mRNA after combined stimulation with IFN-gamma and IL-4. However, in JIJOYE cells, there was a dissociation between the surface expression of Fc epsilon R2 and Fc epsilon R2 mRNA treated with IFN-gamma plus IL-4. In these cells. IFN-gamma even down-regulated the IL-4-induced expression of surface Fc epsilon R2. Stimulation of JIJOYE cells with both IFN-gamma and IL-4 resulted in the increase of the IgE-BF in the supernatant, suggesting that IFN-gamma enhanced the release of IgE-BF from Fc epsilon R2. The results indicated that Fc epsilon R2 and IgE-BF expression is regulated by IFN-gamma at least on two different levels: on transcriptional levels and the levels of cleavage of the surface Fc epsilon R2 to release soluble Fc epsilon R2 (IgE-BF). Ligands binding to the Fc epsilon R2 such as IgE and anti-Fc epsilon R2 mAb enhanced the surface expression of Fc epsilon R2 on these Fc epsilon R2(+) cell lines. This was mainly due to the surface accumulation of the receptors on JIJOYE and U937. However, the stimulation of ED by H107 and anti-Fc epsilon R2 mAb significantly enhanced the mRNA expression, indicating that Fc epsilon R2 synthesis may also be up-regulated by the specific ligands in some cell types.

Antibodies, Monoclonal↗
PubMed1988

Differential modulation of 1-beta-D-arabinofuranosylcytosine metabolism by hydroxyurea in human leukemic cell lines.

The ability of hydroxyurea (HU) to modulate 1-beta-D-arabinofuranosylcytosine (Ara-C) metabolism was investigated in human leukemic cell lines. Exposure of HL-60 cells to 1 mM HU enhanced the accumulation of Ara-CTP up to 2.5-fold, whereas HU did not have significant effects on Ara-C metabolism in CEM cells. In addition, two adenine nucleosides, deoxyadenosine (dAdo) and 9-beta-D-arabinofuranosyladenine (Ara-A), which are known to be activated by deoxycytidine (dCyd) kinase as Ara-C, were more effectively phosphorylated after the addition of HU only in HL-60 cells. However, the changes of intracellular dCTP and TTP pools induced by HU, i.e. decrease in dCTP and increase in TTP, were the same in both cell lines. Finally, dCyd production under normal culture conditions was at least 3- to 4-fold higher in HL-60 cells and was inhibited significantly by HU administration. These results suggest that the modulation of Ara-C metabolism by HU occurs at the level of dCyd kinase through the regulation of de novo dCyd generation.

Arabinofuranosylcytosine Triphosphate↗
PubMed1988

Postnatal changes in plasma burst-promoting activity (BPA) levels in preterm infants.

Two-stage cell culture assays were used to determine burst-promoting activity (BPA) levels in the plasma of untransfused premature infants during the early anaemic period. The plasma BPA levels decreased during the early phase of the postnatal fall in haemoglobin and the mean plasma BPA levels at 2 and 4 weeks of age were significantly lower (24 +/- 9% and 20 +/- 14%) than those of normal adults (53 +/- 17%). After 8 weeks of age, plasma BPA levels increased markedly in correlation with the recovery of erythropoiesis. Inhibitors of erythroid colony growth were not significantly elevated in the plasma of premature infants. These results suggest that BPA may act as a regulator of erythropoiesis in preterm infants along with erythropoietin.

Adult↗
PubMed1988

Effect of thyroid hormones on benzodiazepine receptors in neuron-enriched primary cultures.

The effect of administration of thyroid hormones on central benzodiazepine receptors was investigated using neuron-enriched primary cultures obtained from the neopallium of 16-day-old embryonic rats. Addition of L-triiodothyronine for 3 days decreased the maximal number of benzodiazepine receptor binding sites without any change in affinity at 10(-5) and 10(-6) M. L-Thyroxine administered for 3 days had the same effect at 10(-5) M. No significant change was observed over periods of less than 3 days, a finding indicating that this inhibition was not a direct in vitro effect. This down-regulation seems to be a direct modulatory effect of thyroid hormones on cerebral cortical neurons. Addition for 3 days of D-thyroxine and D-triiodothyronine, which are physiologically inactive isomers of the thyroid hormones, did not induce any significant alterations in benzodiazepine receptors. The decrease in number of cerebral cortical neuronal benzodiazepine receptors due to L-isomers of thyroid hormones may be related to the convulsions and anxiety observed in thyrotoxicosis in humans.

Animals↗
PubMed1988

Plasma atrial natriuretic polypeptide concentration in healthy children from birth to adolescence.

We measured plasma atrial natriuretic polypeptide concentrations in the umbilical artery and vein, and peripheral veins of healthy children from birth to adolescence to establish the normal range. The plasma atrial natriuretic polypeptide concentration in the umbilical artery (mean +/- SD, 51.0 +/- 21.4 fmol/ml) was significantly higher than that in the umbilical vein (18.1 +/- 13.5 fmol/ml) in neonates after vaginal delivery. Also neonates aged 5 days or less had a significantly high concentration in the peripheral vein (60.7 +/- 29.4 fmol/ml). There was no significant difference in atrial natriuretic polypeptide concentrations in the peripheral veins between older children and adults. The concentrations in children aged more than 5 days and adults aged 20-34 years were 14.4 +/- 7.4 fmol/ml and 10.0 +/- 4.8 fmol/ml, respectively. However, the atrial natriuretic polypeptide concentration in the umbilical artery was not increased in three neonates delivered by caesarean section although they had a high concentration in the peripheral vein 24 hours after birth.

Adolescent↗
PubMed1988

Cranial computed tomographic and electroencephalographic abnormalities in children with post-hemiconvulsive hemiplegia.

Twenty-five children with post-hemiconvulsive hemiplegia, who had had epileptiform discharges on EEG, were followed for over 5 years. Twenty-two of them developed the hemiconvulsion-hemiplegia-epilepsy syndrome. The computed tomographic (CT) findings were: marked hemispheric atrophy in 13 cases; moderate or slight hemispheric atrophy in 4; focal atrophy or porencephaly in 4, and a normal scan in 4. The electroencephalographic (EEG) findings showed residual asymmetry of hemispheric amplitudes in 15 cases. Epileptiform discharges on EEG were found on the ipsilateral side (the damaged hemisphere) in 13 cases, the contralateral side (the undamaged hemisphere) in 9, and on both sides in 3. As to the correlation between CT and EEG abnormalities, 8 of 13 cases with marked hemiatrophy on CT had contralateral epileptiform discharges on EEG, and the converse was more pronounced: 8 of 9 cases with contralateral epileptiform discharges had marked hemiatrophy on CT. Contralateral epileptiform EEG abnormalities were observed in the patient with severe hemispheric brain damage.

Adolescent↗
PubMed1988

IgE receptor-bearing lymphocytes in allergic and nonallergic children.

Using a monoclonal anti-human IgE receptor (Fc epsilon R) antibody, the percentage of Fc epsilon R(+) cells among peripheral blood lymphocytes in children with or without allergic disorders was determined. The percentage of Fc epsilon R(+) cells in 63 nonallergic children was 4.3 +/- 1.5%, which did not vary with age and was equal to that of adults (4.2 +/- 1.2%). Allergic younger children (0-2 yr) showed a significantly higher percentage of Fc epsilon R(+) cells (7.7 +/- 3.0%) than nonallergic younger children (0-2 yr) (4.0 +/- 1.3%, p less than 0.001). Similarly, in allergic younger children, serum IgE levels (geometric mean = 58.9 IU/ml) were also significantly higher than those of nonallergic younger children (geometric mean = 2.0 IU/ml) (p less than 0.01). A positive correlation between the percentages of Fc epsilon R(+) cells and serum IgE levels was observed (Spearman rank = 0.88, p less than 0.01] in eight allergic younger children (0-2 yr) with serum IgE levels higher than 100 IU/ml. The increase in the percentage of Fc epsilon R(+) cells in allergic younger children (0-2 yr) was not a secondary phenomenon caused by serum IgE because serum IgE levels in these children were much lower than the concentration at which IgE enhance Fc epsilon R expression on lymphocytes. In conclusion, Fc epsilon R(+) lymphocytes may play a regulatory role in IgE synthesis in allergic younger children (0-2 yr).

Adolescent↗
PubMed1988

Hypothalamic-pituitary function in growth hormone-deficient patients with pituitary stalk transection.

We compared 1.5 T magnetic resonance (MR) image findings with hypothalamic-pituitary function in 11 patients with idiopathic pituitary dwarfism, each of whom had a history of perinatal abnormalities, and 1 patient with posttraumatic pituitary dwarfism. MR imaging revealed transection of the pituitary stalk in all patients and the formation of an ectopic posterior lobe at the proximal stump in 9 patients, none of whom had polydipsia or polyuria. Three patients without an ectopic posterior lobe had diabetes insipidus. The 5 patients who had small pituitary glands (less than 2 mm in height) had hypothyroidism with low serum TSH concentrations and low serum cortisol responses to insulin-induced hypoglycemia; however, 7 patients with normal-sized pituitary glands had normal thyroid and adrenal function. The serum GH response to GHRH did not correlate with the size of the pituitary gland. The patients with small pituitary glands had delayed or prolonged serum TSH responses to TRH and impaired serum LH and FSH responses to GnRH; 4 of the patients with normal-sized pituitary glands had normal serum TSH, LH, and FSH responses. Only 2 patients had high basal serum PRL concentrations. The endocrinological data suggest that reestablishment of the hypothalamo-hypophyseal portal circulation, which cannot be seen by MR imaging, may occur. We suggest that the primary cause of idiopathic pituitary dwarfism in many patients is injury to the pituitary stalk at birth.

Adolescent↗
PubMed1988

Regulation of Fc epsilon receptor expression on a human monoblast cell line U937.

Fc epsilon receptor (Fc epsilon R) expression on several human cell lines (U937, RPMI 8866, HL 60, THP-1, and Molt 4) and its regulation were examined by immunofluorescent analysis using a monoclonal anti-human Fc epsilon R antibody, H107. Phorbol ester (PMA), recombinant gamma interferon (IFN-gamma) and H107 itself enhanced Fc epsilon R expression on a FC epsilon R positive cell line U937, whereas these reagents did not induce FC epsilon R expression on the Fc epsilon R negative cell lines, Molt 4, HL 60 and THP-1. Dexamethasone not only suppressed by 50% the spontaneous Fc epsilon R expression on U937 cells but also completely inhibited the enhancement of their Fc epsilon R expression on U937 cells induced by PMA, IFN-gamma or H107. Dexamethasone caused a little suppression of Fc epsilon R expression by RPMI 8866 cells. The results showed that Fc epsilon R expression on a human monoblast cell line U937 was up- or down-regulated by a variety of physiological or pharmacological agents. These experimental systems provide a good model for the investigation of the regulatory mechanisms of Fc epsilon R expression.

Antibodies, Monoclonal↗
PubMed1988

[Clinical evaluation of sultamicillin fine granules in pediatric patients].

The clinical efficacy and the safety of sultamicillin (SBTPC) fine granules, which is a semisynthetic beta-lactam antibiotic for oral use with ester linked ampicillin (ABPC) and sulbactam (SBT), a beta-lactamase inhibitor, in a ratio of 1:1, were evaluated in 31 patients with ages from 6 months old to 10 years and 4 months old with various bacterial infections. The results obtained are summarized as follows. 1. In a pharmacokinetic study with a dose level of 10 mg/kg SBTPC, serum levels reached a peak in 1 hour after oral administration, with peak levels of 3.94 micrograms/ml for ABPC and 4.08 micrograms/ml for SBT. Half-lives of ABPC and SBT were 64.8 minutes and 63.6 minutes, respectively. The urinary excretion of ABPC over 6 hours was 66.2% and that of SBT was 60.4%. 2. SBTPC fine granules were administered orally to 1 patient with bronchitis, 9 patients with bronchopneumonia, 7 patients with tonsillitis, 4 patients with scarlet fever, 1 patient each with pharyngitis, otitis media, purulent parotitis, and urinary tract infection and 6 patients with skin and soft tissue infections at daily dosage levels of 26.1-31.6 mg/kg divided into 3 or 4. Clinical evaluations of these 31 patients were as follows, excellent: 20 patients, good: 10 patients, poor: 1 patient. The efficacy rate was 96.8%. 3. Diarrhea was observed in a patient with otitis media on the fifth day of SBTPC administration. No other clinical adverse reaction was observed in any of the remaining 30 patients. No abnormal laboratory data was found in any of 23 patients who were subjected to laboratory examinations for safety.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1988

Changes in sensitivity to anticancer drugs during TPA-induced cellular differentiation in a human T-lymphoblastoid cell line (MOLT-4).

After four days of treatment with 10(-8) M TPA, differentiation of the human T-lymphoblastoid cell line MOLT-4 was induced along the T cell lineage, confirmed by a fall in adenosine deaminase and 5'-ectonucleotidase and a rise in purine nucleoside phosphorylase activity. TPA-treated cells became resistant to the cytotoxic effects of 1-beta-D-arabinofuranosylcytosine (Ara-C), 9-beta-D-arabinofuranosyladenine (Ara-A), and 2-chlorodeoxyadenosine. This was, in part, due to the altered cell cycle distribution (accumulation of cells in the G1 phase), since the toxicity of Ara-C and Ara-A is S phase specific. The diminished rate of Ara-C transport concomitant with Ara-CTP formation after TPA treatment is considered to be the biochemical basis for this acquired resistance.

Antineoplastic Agents↗
PubMed1988

Low burst-promoting activity (BPA) production by cord mononuclear cells is due to functional immaturity of monocytes.

Cord blood mononuclear cells produced lower burst-promoting activity (BPA) than adult peripheral blood mononuclear cells when stimulated with phytohemagglutinin (PHA). In order to examine the cellular basis of the low production of BPA by PHA-stimulated cord blood mononuclear cells in the context of the functional immaturity of T cells or monocytes, we studied BPA production by T cells or monocytes from cord blood and adult peripheral blood. Cord T cells produced as much BPA as adult T cells. Monocytes themselves did not produce significant BPA at the concentration used in this experiment (1 x 10(5)/ml). BPA production by adult T cells was significantly enhanced by the presence of autologous monocytes. BPA production by cord T cells was also enhanced by the presence of adult monocytes but not by that of cord monocytes. Cord monocytes did not enhance BPA production by adult T cells either. These results indicate that cord monocytes are primarily responsible for the low BPA production by PHA-stimulated cord mononuclear cells.

Erythropoiesis↗
PubMed1987

Prevention of adriamycin-induced interphase death by 3-aminobenzamide and nicotinamide in a human promyelocytic leukemia cell line.

Adriamycin caused significant interphase death in HL-60 cells during six hours of incubation, which was abolished by the poly(ADP-ribose) polymerase inhibitors, 3-aminobenzamide or nicotinamide. Neither agent changed adriamycin uptake by HL-60 cells. Although 3-aminobenzamide did not alter the number of DNA strand breaks caused by adriamycin, it prevented adriamycin-induced depletion of intracellular NAD+ and ATP, and maintained energy charge. These findings suggest that the activation of poly(ADP-ribose) synthesis plays an important role in the adriamycin-induced interphase death of proliferating HL-60 cells.

Benzamides↗