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Biomedical subjects

Y Honma

Publications and source records attributed to Y Honma.

At least 271 records · Page 15Linked to original sources
PubMed1987

Inhibition of messenger RNA transcriptional activity in ML-1 human myeloblastic leukemia cell nuclei by antiserum to a c-myb-specific peptide.

Antiserum to a synthetic peptide that defines a hydrophilic region within the putative c-myb translation product was prepared in the rabbit. In lysates from exponentially growing ML-1, human myeloblastic leukemia cells, the antiserum ("anti-myb") reacted with five proteins of Mr 58,000, 75,000, 85,000, 90,000 and 105,000. Of these, only p75 and a trace of p85 were detected, by immunoblotting, in extracts derived from ML-1 cell nuclei. The proteins p58, p75 and p90 were present in readily detectable amounts only in the relatively immature myeloid cell lines ML-1 and HL-60, whereas in the more mature myeloid cell line THP-1 and in the lymphoid line BALL-1 only traces of these proteins were found. p85 and p105 were detected in lysates from all cell lines tested, including myeloid and lymphoid leukemia cells and mouse 3T3 cells. In lysates from ML-1 cells induced to differentiate to monocyte/macrophages or to granulocytes, the concentrations of p58 and p75 decreased in parallel with the cell population moving to maturity; in completely mature populations these two proteins were no longer detectable. In ML-1 cells arrested in G1 by serum depletion, the amount of p58 and p75 and to a smaller extent that of p90 was decreased, whereas the concentration of p85 and p105 remained unchanged. In nuclei from exponentially growing ML-1 cells, the antiserum or its derived immunoglobulin fraction ("anti-myb IgG") inhibited mRNA transcriptional activity by 30%. DNA synthesis was not affected. In contrast, in nuclei from differentiated ML-1 cells, the mRNA transcriptional activity was not significantly inhibited by anti-myb IgG. Similarly, in nuclei from ML-1 cells arrested largely in G1 by serum depletion for 2 days, mRNA transcriptional activity was inhibited by only 11%. Upon supplementation with serum, the mRNA transcriptional activity inhibitable by anti-myb IgG increased in parallel with the increasing rate of cell growth. The difference in total mRNA transcriptional activity observed in nuclei from cells of different growth rate was accounted for by the difference in transcriptional activity inhibitable by anti-myb IgG.(ABSTRACT TRUNCATED AT 400 WORDS)

Antibody Specificity↗
PubMed1987

Control of proliferating potential of myeloid leukemia cells during long-term treatment with vitamin D3 analogues and other differentiation inducers in combination with antileukemic drugs: in vitro and in vivo studies.

Growth inhibition of murine and human myeloid leukemia cells by differentiation inducers during long-term culture was examined to improve the strategy for therapy of myeloid leukemia by differentiation inducers. When the effect of 1 alpha,25-dihydroxyvitamin D3, a typical differentiation inducer, on proliferation of mouse myeloid leukemia M1 cells was examined at a constant product of time and concentration (480 nM in 20 days), the continuous treatment with 24 nM 1 alpha,25-dihydroxyvitamin D3 was the most effective for inhibition of cell proliferation. After 20 days, the cumulative cell number was reduced about 3 X 10(5) times by continuous treatment with 24 nM 1 alpha,25-dihydroxyvitamin D3. Similar results were obtained when M1 cells were treated continuously with dexamethasone. M1 cells resistant to 1 alpha,25-dihydroxyvitamin D3 appeared about 25 days after the start of continuous treatment with 24 nM 1 alpha,25-dihydroxyvitamin D3. On the other hand, when M1 cells were treated continuously with 1 alpha,25-dihydroxyvitamin D3 and noncytotoxic doses of antileukemic drugs such as 1-beta-D-arabinofuranosylcytosine and daunomycin, resistant cells did not appear for at least 35 days. A similar effect of 1 alpha,25-dihydroxyvitamin D3 and antileukemic drugs on cell proliferation was observed with the human monoblast-like cell line U937. The survival of syngeneic SL mice inoculated with M1 cells was prolonged more by treatment with both 1 alpha-hydroxyvitamin D3 and daunomycin than by treatment with either drug alone. These results suggest that continuous treatment with both differentiation inducers and certain antileukemic drugs may be more effective therapeutically than treatment with a differentiation inducer alone.

Animals↗
PubMed1987

Prediction and evaluation of brainstem function by auditory brainstem responses in patients with uncal herniation.

Serial measurements of auditory brainstem-evoked responses (BERs) were conducted in 15 patients with supratentorial mass lesions. Significant prolongation of the latency of wave V BERs, which originates in the inferior colliculus, occurred when the intracranial pressure (ICP) approached 30 mmHg. In four of five patients whose BERs were measured before pupillary changes, a significant lengthening of wave V latency was observed prior to clinical manifestation of uncal herniation. These results suggest that immediate medical or surgical decompression of ICP should be performed when ICP approaches 30 mmHg with significant prolongation of wave V latency.

Adult↗
PubMed1987

Differentiation of blasts from patients in myeloid crisis of chronic myelogenous leukemia by in-vivo and in-vitro plicamycin treatment.

Two cases in myeloid blast phase of chronic myelogenous leukemia (CML) responded to treatment with plicamycin alone. Their total white blood cell (WBC) count and immature myeloid cells fell in one case rapidly and in the other gradually. Approximately two to three weeks after initiation of plicamycin their total WBC count began to rise again, whereas the mature myeloid cells remained constant throughout the treatment. These results suggest that plicamycin may be effective in suppressing proliferation of blasts and promoting their maturation in the myeloid blast phase of CML, but that plicamycin alone may not be effective enough to sustain duration of response.

Adult↗
PubMed1987

Constrictive structural elements in human cerebral arteries following aneurysmal subarachnoid haemorrhage.

Histoimmunological, histochemical, and histological studies were conducted on cerebral arteries from four living patients with a recent aneurysmal subarachnoid haemorrhage. There appeared to be a correlation between the severity of vasospasm and the magnitude of pathological findings. Large myofibroblast cells and type V collagen within the medial layer were abundant in arteries showing marked vasospasm, but were less conspicuous in those showing milder involvement. Intracranial arteries from patients who died from non-cerebral causes did not demonstrate these changes. In ruptured vessels, there was also a positive fluorescence for actin-myosin filaments in layers of the arterial wall other than the media. It is postulated that the intimal and adventitial actin-myosin, myofibroblasts and type V collagen may contribute to cerebral vasospasm by holding the damaged vessel in a contracted phase during the healing period.

Adult↗
PubMed1987

Vascularization of the hypothalamo-hypophysial complex in Japanese elasmobranchs: a scanning electron microscope study of blood vascular casts.

To study in detail vascularization in the hypothalamo-hypophysial complex in some Japanese elasmobranchs, injection casts of blood vessels were observed by scanning electron microscopy. Materials used were a gummy shark (Mustelus manazo), a cloudy dogfish (Scyliorhinus torazame) and a skate (Raja porosa). The vascular supply to the hypothalamo-hypophysial region of the elasmobranchs is carried out by the inferior hypothalamic arteries and their branches that originate from the internal carotid artery. In the gummy shark, a pair of inferior hypothalamic arteries send several branches to the median eminence running along the anterolateral sides of the distal adenohypophysis. These branches form the capillary plexus, displaying anastomosis and convolution at the ventral surface of the median eminence. The plexus assumes capillary glomeruli at the lateral region of the posterior median eminence. Numerous branches derived from the plexus are directed backward through the pars distalis, join with the capillary net work (which develop in the neuro-intermediate lobe) and are finally gathered together to form a thick hypophysial vein. The ventral lobe receives several arterial branches from the internal carotid arteries and carotid artery to form a unique vascular bed. Therefore, it is assumed that in elasmobranchs the hypothalamic control of the ventral lobe is weaker than that of adenohypophysial components.

Animals↗
PubMed1987

Production by undifferentiated myeloid leukemia cells of a novel growth-inhibitory factor(s) for partially differentiated myeloid leukemic cells.

Mouse monocytic Mm-A cell line is a highly leukemogenic variant cell line of the monocytic and non-leukemogenic Mm-1 cell line, which developed spontaneously from mouse myeloid leukemia M1 cells. Growth-inhibitory factor (GI factor) for Mm-A cells was found in conditioned medium (CM) of differentiation inducer-resistant myeloblastic M1 cells (clone R-1). The R-1 cells were cultured with or without 2% calf serum for 2 days, and the CM was fractionated with 50% ammonium sulfate and used as the GI factor preparation (termed R1CM). When Mm-A cells were cultured with 5% (v/v) R1CM for 3 days, their growth was inhibited about 80%. This inhibition of Mm-A cell growth by R1CM was irreversible. This GI factor also inhibited the growth of M1 cells that had been pretreated with inducer and had expressed some differentiation-associated properties but still retained a proliferative capacity. In contrast, it scarcely inhibited the growth of untreated M1 cells. The GI factor inhibited the growth of other mouse monomyeloblastic leukemic WEHI-3B D+ cells pretreated with a differentiation inducer, retinoic acid, and mouse monocytic leukemia J774.1 cells. However, it did not affect the growth of human monocytic (U937 and THP-1) or myeloid (KG-1, ML-1, and HL-60) cell lines. These results suggest that GI factor produced by parent myeloblastic and inducer-resistant M1 cells preferentially inhibits the growth of mouse monocytic leukemia cells in intermediate stages of differentiation from myeloblastic leukemia cells to mature macrophages.

Animals↗
PubMed1987

[Interaction between neurogenic and metabolic factors upon deterioration in cerebrovascular tonus--experimental study on the etiology of cerebral vasoparesis].

It is widely accepted that a tremendous increase in cerebral blood volume (CBV) due to progressive cerebral vasoparesis is an essential to the development of acute brain swelling. This study was designed to determine whether neurogenic and/or metabolic factors are predominant and how these interact with each other in producing cerebral vasoparesis. Fifty-one awake cats immobilized with pancuronium bromide were divided into 4 groups: group I, control; group II, normocapnic hypoxia (PaO2 = 50 mmHg); group III, normoxic hypercapnia (Pa-CO2 = 70 mmHg), and group IV, increased intracranial pressure (ICP = 40 mmHg) by brain compression. Systemic arterial pressure (BP), CBV (photoelectric method), and ICP (epidural pressure) were continuously recorded. The dorsomedial hypothalamic nucleus (DM) and the reticular formation of the midbrain (MB-RF) were bilaterally coagulated by a stereotaxic technique (3mA, 1 min). Therefore alterations in cerebrovascular tonus created by destruction of the cerebral vasomotor centers were examined in the animals with metabolically induced cerebral vasodilatation to various degree's. In group I, vasomotor center destruction resulted in an immediate and transient decrease in BP (DM; -14.1 +/- 6.7 mmHg, MB-RF; -10.2 +/- 4.8 mmHg) and simultaneous increase in CBV and ICP (DM; 7.6 +/- 7.0 mmHg, MB-RF; 6.0 +/- 5.6 mmHg) for 3 to 4 minutes. Increase in ICP by destruction of vasomotor centers reduced significantly in group II (DM; 2.3 +/- 2.6 mmHg, MB-RF; 1.6 +/- 1.2 mmHg) and reduced slightly in group IV (DM; 7.5 +/- 4.0 mmHg, MB-RF; 4.8 +/- 3.2 mmHg). In these 3 groups, autoregulation of cerebral blood flow and CO2 vasoreactivity were not changed by destruction of vasomotor centers.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Aggregation of the smooth muscle cells found in certain hemopoietic organs and tissues of the stingray, Dasyatis akajei (Elasmobranchii, Chondrichthyes).

A combined light and electron microscopic study revealed that there are conspicuous aggregations of smooth muscle cells in several hemopoietic organs and tissues such as in the Leydig (esophageal) and epigonal organs, diencephalic choroid plexus and perihypophyseal connective tissue sheath of the stingray, Dasyatis akajei. These cells were gathered in bundles of varying caliber or arranged concentrically around a central focus, but neither innervation nor gap junction was found. In some of the concentrically arranged cells, signs of degeneration were noticed. The possible origin of these structures is discussed in relation to the vascularity of the loose connective tissue.

Animals↗
PubMed1986

Enhancement by hemin of the sensitivity of K562 human leukemic cells to 1-beta-D-arabinofuranosylcytosine.

The sensitivity of human leukemia K562 cells to cancer chemotherapeutic drugs during induction of erythroid differentiation of the cells by hemin was examined. Treatment with hemin greatly increased the sensitivity of the cells to 1-beta-D-arabinofuranosylcytosine (ara-C) but did not affect their sensitivities to other chemotherapeutic drugs, including Adriamycin, daunomycin, hydroxyurea, methotrexate, and vincristine. Thymidine and deoxyguanosine, which are known to potentiate the antileukemic effects of ara-C in K562 cells, also induced erythroid differentiation of K562 cells, but other inducers, such as sodium butyrate and delta-aminolevulinic acid, did not increase the sensitivity of K562 cells to ara-C. Hemin did not enhance the sensitivity to ara-C of other leukemia cell lines (Friend erythroleukemic cells, myeloid leukemic M1 cells, and promyelocytic leukemia HL-60 cells). These results indicate that some inducers of erythroid differentiation of K562 cells potentiate the antileukemic effect of ara-C on K562 cells.

Aminolevulinic Acid↗
PubMed1986

Mechanism of interaction between antineoplastic agents and natural differentiation factors in the induction of human leukemic cell maturation.

DNA-specific agents have the capacity to induce the maturation of ML-1 human myeloblastic leukemia cells to monocyte/macrophages if adequate concentrations of fetal bovine serum or mitogen-stimulated human leukocyte-conditioned medium (CM) are present in the culture medium. Fetal bovine serum and CM contain specific differentiation-inducing factors that, in conjunction with the drugs, bring about cell maturation. To examine the mechanism by which this interactive effect occurs, ML-1 cells were exposed to actinomycin D or daunomycin in various combinations with CM, using concentrations at which neither the drug nor CM, when applied individually, induced maturation to a significant extent. Pretreatment for 3 days with drug followed by treatment for 3 days with CM caused maturation of 75% of the cells, as determined by the appearance of Fc receptors. Other markers of differentiation, including alpha-napthyl acetate esterase, acid phosphatase, and morphology, also reflected the increase in maturation. The simultaneous application of drug and CM was equally effective in inducing differentiation. Pretreatment of the cells with CM followed by treatment with drug failed to induce maturation, whereas pretreatment with CM followed by a second application of CM caused the expression of Fc receptors in 62% of the cells. In contrast, pretreatment with drug followed by a second application of drug did not induce differentiation significantly. These results indicate that the drug sensitizes the cells to respond to concentrations of CM to which they would otherwise be refractive. The drug-induced sensitization is reversible. At sensitizing drug concentrations, cell viability was preserved but, as measured by radiolabeling for 1 h, total RNA synthesis was decreased by 38% and mRNA synthesis by 87%. At these drug concentrations, the synthesis of mRNA specified by all seven oncogenes examined (myb, myc, abl, fos, N-ras, sis, erb B) was decreased by 15-60%. The administration of CM subsequent to drug caused a further decrease of some mRNA levels (c-myb, c-myc) but increased the level of others (c-fos). The drug-induced lowering of mRNA levels is considered to inhibit the synthesis of proteins specifically required for G1-S transit and maintenance of the proliferation program, amplifying, thereby, the maturation signal emitted by the differentiation factors present in serum and in CM. As a result, expression of the maturation program is initiated.

Antineoplastic Agents↗