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Biomedical subjects

Y Honma

Publications and source records attributed to Y Honma.

At least 253 records · Page 14Linked to original sources
PubMed1989

Granulocyte-colony stimulating factor and retinoic acid cooperatively induce granulocyte differentiation of acute promyelocytic leukemia cells in vitro.

The interaction of granulocyte-colony stimulating factor (G-CSF) and retinoic acid (RA) in proliferation and differentiation of acute promyelocytic leukemia (APL) cells was examined. G-CSF stimulated proliferation of APL cells at concentrations of 0.1 to 50 ng/ml in a dose dependent manner. More than 10(-8) M RA induced granulocytic differentiation of APL cells. Although G-CSF induced lysozyme activities in APL cells, it alone did not induce terminal differentiation of APL cells. G-CSF significantly enhanced the RA-induced granulocytic differentiation of APL cells in vitro. Enhancement by G-CSF was not due to the prolongation of survival of RA-induced differentiated cells, but the differentiation-inducing effects of G-CSF might be evident only in the presence of RA. Since G-CSF has a potential to induce the granulocytic differentiation of myeloid leukemia cells, G-CSF in combination with RA may be applicable in differentiation induction therapy for some types of myeloid leukemia.

Adult↗
PubMed1989

Inhibitory action of transforming growth factor-beta on induction of differentiation of myeloid leukemia cells.

The effect of transforming growth factor-beta (TGF-beta) on induction of differentiation of mouse myeloid leukemia M1 cells was investigated. TGF-beta 1 induced adherence of M1 cells to plastic dishes and inhibited their proliferation. However, it did not induce differentiation-associated properties, such as phagocytic activity, lysozyme activity or morphological maturation. TGF-beta 1 also caused dose-dependent inhibition of dexamethasone-induced differentiation of M1 cells. The inhibitory activity of TGF-beta 1 was 20 times that of TGF-beta 2 on M1 cells. These results suggest that TGF-beta 1 inhibits proliferation and dexamethasone-induced differentiation of M1 cells by interacting with receptors that can distinguish between TGF-beta 1 and TGF-beta 2. TGF-beta 1 had a much lower inhibitory effect on the growth of a variant M1 cell clone, which was resistant to differentiation inducers, and it did not induce adherence of the resistant M1 cells.

Animals↗
PubMed1989

Comparison of intimal platelet accumulation in cerebral arteries in two experimental models of subarachnoid hemorrhage.

Intimal accumulation of indium-111-labeled platelets in the middle cerebral arteries was examined in two different models of experimental subarachnoid hemorrhage (SAH) in the cat. SAH was produced in 7 subjects by a transorbital rupture of the right middle cerebral artery (RMCA) and in 10 subjects by the transorbital cisternal injection of 2 ml of autologous arterial blood around the RMCA. Animals in both experimental groups were sacrificed at 2, 4, 24, and 48 hours after SAH. The radioactivity (in counts per minute) of the RMCA segment was divided by that of the left middle cerebral artery (LMCA) to produce a radioactivity ratio (RMCA/LMCA). This radioactivity ratio was determined for each animal and was scored as positive if it was 1.25 or greater, and as negative if it was less than 1.25. The scores derived from the radioactivity ratios in both experimental SAH groups were mostly positive (86 and 70%, respectively) and were significantly different (P less than 0.05) from those of intact controls (n = 7) or sham-operated controls (n = 5; n = 4). There was, however, no significant difference (P = 0.35) between the scores of the two experimental groups in the first 48 hours after SAH. The results indicate that subarachnoid blood placed upon the adventitial surface of intact cerebral arteries activates platelet aggregation to a degree comparable to that which occurs after mechanical vessel rupture in the acute stages of SAH. We suggest that the noxious agents responsible for arterial injury and subsequent intimal platelet aggregation after SAH exert their influence primarily from the abluminal surface of the cerebral artery.

Animals↗
PubMed1989

Synthesis and antitumor activity of new amphiphilic alkylglycerolipids substituted with a polar head group, 2-(2-trimethylammonioethoxy)ethyl or a congeneric oligo(ethyleneoxy)ethyl group.

A new series of amphiphilic 1-octadecyl glycerolipids (eleven compounds, 1a-k) were designed and synthesized, in which the 3-phosphocholine portion of platelet-activating factor (1-alkyl-2-acetyl-sn-glycero-3-phosphocholine, PAF) was replaced by the 2-(2-trimethylammonioethoxy)ethyl group and congeneric groups having oligo(ethyleneoxy)ethyl bridges of various lengths at position 3, together with modification at position 2 (lower alkyl, acetonyl, acetoacetyl, carboxymethyl and pyrimidin-2-yl groups). These ether lipids, characterized by a nonphosphorus lysoglycerolipid structure, showed potent antitumor activity in vitro (human promyelocytic leukemia cells, HL-60, and human epidermoid carcinoma cells, KB) and in vivo (mouse sarcoma S180 and mouse mammary carcinoma MM46). Maximal in vitro potency was obtained with 1-O-octadecyl-2-O-(2-pyrimidinyl)-3-O-[2-(2-trimethylammonioethoxy )ethyl] glycerol (1g; IC50 values for both HL-60 and KB were 0.32 microgram/ml, indicating a higher activity than alkyl-lysophospholipid, ET18-OMe). Several appropriately 2-substituted 1-octadecylglycerolipids with the 3-[2-(2-trimethylammonioethoxy)ethyl] group (e.g., methyl, 1b; butyl, 1f; 2,2,2-trifluoroethyl, 1j; and acetonyl, 1k) showed a potent life-span-prolonging effect on mice with ascites sarcoma S180 and on those with mammary carcinoma MM46, when administered intraperitoneally at 16.5 and 12.5 mg/kg/d, respectively. Compounds 1b and 1k showed definite tumor growth inhibition against solid sarcoma S180 in mice, whether given p.o. or i.v. at 16.5 mg/kg/d. Studies on the structure-activity relationships indicate that the metabolic stability to phospholipase C or related enzymes is at least partly responsible for the potent antitumor activity of this series of ether lipids.

Animals↗
PubMed1989

[A case of thymoma associated with prostatic cancer].

A case of prostatic cancer treated with an LH-RH analogue depo-preparation was found to have a mediastinal thymoma which was later removed by surgery. The association of thymoma and prostatic cancer has not been documented in the world literature, and it remains to be elucidated whether the occurrence of the both tumors is a coincidence or etiologically inter-related.

Adenocarcinoma↗
PubMed1989

[Testicular endocrine function in patients with prostatic cancer receiving medical castration by long-term administration of LH-RH agonists].

Six patients with advanced prostatic cancer who had been treated by long-term administration of LH-RH agonistic preparations (Buserelin or Leupron) were tested for their pituitary-testicular endocrine functions. Serum levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone (T), prolactin (PRL), estradiol (E2) and dihydrotestosterone (DHT) were measured consecutively. In all medically castrated patients, serum levels of LH, FSH, T, DHT and E2 were suppressed and particularly serum T levels were below the castration level of 1.0 ng/ml. On the other hand, serum PRL levels were unchanged after the long-term treatment with the agonists. Serum LH and FSH levels failed to respond to LH-RH stimulation after the treatment, whereas serum T responded to stimulation by human chorionic gonadotropin (hCG) to various degrees. It was remarkable that, in 4 out of 6 medically castrated patients treated up to more than 3 years, serum T response levels above 1.0 ng/ml were noted. It is suggested that testicular endocrine function to secrete T and DHT in patients under treatment with long-term LH-RH agonist administration are still preserved in response to hCG stimulation.

Adenocarcinoma↗
PubMed1989

[An autopsy case of anoxic encephalopathy caused by transient upper airway obstruction].

We reported the pathological findings of an autopsy case of anoxic encephalopathy, with special reference to the topography of degenerative changes in the nervous system. A 47 year-old man, who had an episode of sudden upper air-way obstruction although his radial artery pulsation was maintained, and then suffered from akinetic mutism and myoclonus for 2 years and 5 months, died of bronchopneumonia. Postmortem examination revealed that, in addition to wide distribution of mild neuronal loss and astrocytosis in the cerebral and cerebellar gray matter, focal pseudolaminer necrosis of the IIIrd and IVth cortical layers was predominantly noticed in the calcarine cortex, pre- and postcentral gyri and transverse temporal cortex. However, the cortical architecture of the Ammon's horn, arterial boundary zones and depths and sides of sulci was not involved. This topography of neuronal degeneration was considered to correspond with those of methyl-mercury intoxication. However, his history and neurological examination before the episode denied the intoxication. Conclusively, the characteristic distribution of the brain damage in this case are resulted from the episode of pure anoxic anoxia, suggesting that the anoxic encephalopathy would make up a different involvement pattern of the brain from those of ischemic encephalopathy.

Airway Obstruction↗
PubMed1989

[An autopsy case of thrombotic thrombocytopenic purpura--topography of the vascular lesion in the central nervous system].

We reported the pathological findings of an autopsy case of thrombotic thrombocytopenic purpura, with special reference to the topography of vascular lesion in the central nervous system. Amorphous eosinophilic, PAS-positive thrombi, endothelial proliferation and aneurysmal dilatation of affected vessels were prominent features in the visceral organs such as the heart, kidneys, liver, pancreas, adrenals, thyroid and alimentary tracts. Most of these vascular lesions were restricted to the arteriolar-capillary junctions. There were no thrombi in the lungs as reported previously. In addition, the thrombi were rarely seen in so-called portal vessels existed in the liver, pancreas and anterior pituitary gland. In the central nervous system, there were many vascular lesions similar to those of visceral organs in the cerebral gray matter, brain stem and cerebellar cortex. A few lesions were also seen in the white matter, subarachnoid space and choroid plexus. Many foci of chromatolytic neurons as well as a few petechial hemorrhages and minute infarcts were observed in the parenchyma. The characteristic of the vascular lesions in the cerebral and cerebellar cortex was the sites of thrombi. They were predominantly located at the bifurcation of arterioles, 20-50 microns in diameter, and were numerous in the third or fourth cortical layer of the cerebrum, and in the Purkinje cell layer of the cerebellum. Although the etiology of TTP is still unknown, the characteristic topography of vascular lesions suggests primary endothelial involvement in this disease.

Arterioles↗
PubMed1988

Purification of a factor inhibiting differentiation from conditioned medium of nondifferentiating mouse myeloid leukemia cells.

Mouse myeloid leukemic M1 cells are induced to differentiate by various differentiation inducers. Activity for inhibition of induction of differentiation of M1 cells (I-factor activity) was detected in conditioned medium of variant M1 cell clones that were resistant to differentiation inducers, and this I-factor activity was shown to be closely associated with resistance of the cells to differentiation inducers. In this work, the I-factor was purified to apparent homogeneity from conditioned medium of resistant M1 cells. The purification procedure consisted of ammonium sulfate precipitation, CM-Sepharose CL-6B, Sephadex G-200, reverse-phase high performance liquid chromatography on a C18 hydrophobic support, and high-performance liquid chromatography on a gel filtration column. The factor was analyzed by radioiodination, sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and autoradiography. The purified factor gave a single band of protein with a molecular weight of 68,000 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis which coincided with its biological activity. The concentration of I-factor required for 50% inhibition of dexamethasone-induced differentiation of M1 cells was 24 pM. At its effective concentration it had no effect on cell proliferation, and even at 1.2 nM it did not inhibit colony formation of normal bone marrow cells, suggesting that it was distinct from the inhibitor of normal precursors of macrophages and/or granulocytes.

Animals↗
PubMed1988

Purification of a novel growth inhibitory factor for partially differentiated myeloid leukemic cells.

A novel factor termed growth inhibitory (GI) factor, which specifically inhibits the growth of mouse monocytic leukemia cells including monocytic cell lines (Mm-A and J774.1) and other partially differentiated myeloid leukemic cells, has been purified from conditioned medium of some clones of mouse myeloblastic leukemia M1 cells. The procedure for purification of the GI factor included ammonium sulfate precipitation, CM-Sepharose CL-6B and Sephadex G-200 chromatographies, reverse-phase high-performance liquid chromatography on a C18 hydrophobic support, and high-performance liquid chromatography on a gel filtration column. The purified factor gave a single band of protein with a molecular weight of 25,000 on sodium dodecyl sulfate-polyacrylamide gel. A concentration of 8 X 10(-10) M GI factor was required for 50% inhibition of growth of Mm-A cells. On chromatofocusing, the GI activity was eluted with Polybuffer 96/acetic acid at pH 8.2-8.4. The purified GI factor markedly inhibited growth of mouse bone marrow cells stimulated by macrophage colony-stimulating factor. The GI factor appeared to be a unique cytokine unrelated to known cytokines such as the tumor necrosis factor, interferons, and oncostatin M.

Animals↗
PubMed1988

Occurrence of lymphohaemopoietic tissue in the meninges of the stingray Dasyatis akajei (Elasmobranchii, chondricthyes).

The cytoarchitecture of the lymphohaemopoietic masses occurring in the "meninx primitiva" of the stingray Dasyatis akajei (Elasmobranchii, Chondricthyes) has been analyzed by light and scanning and transmission electron microscopy. Lymphohaemopoietic aggregates showing similar morphologies occurred along all the central nervous system, but they were more frequent in the telencephalon, diencephalon, and mesencephalon. In each aggregate, the granulopoietic tissue appeared in a fibroblastic stroma surrounding the large blood vessels, and the lymphoid components were present in a reticular network. Developing and mature eosinophils and heterophils--as well as lymphocytes, monocytes, macrophages, and plasma cells--are the main free cells present in these meningeal aggregates. The remarkable intimate association between macrophages and lymphoid cells to form close cell clusters suggests some immunological capacity for the meningeal lymphohaemopoietic tissue. According to their capacities, presence of lymphoid tissue, and histological organization, the meningeal lymphohemopoietic aggregates of Dasyatis akajei resemble other lymphomyeloid aggregates associated with cranium and choroid plexuses in Holocephali and Ganoidei. The phylogenetical relationships of these aggregates with mammalian bone marrow are discussed.

Animals↗
PubMed1988

Pathological changes in cerebral arteries following experimental subarachnoid hemorrhage: role of blood platelets.

The role of blood platelets in producing early intimal changes in cerebral arteries following subarachnoid hemorrhage (SAH) was examined by using 18 cats. Experimental SAH was produced by a rupture of the proximal portion of the right middle cerebral artery. Following SAH, the scanning electron microscope revealed that structural alterations in the intimal layer of major cerebral arteries occurred as early as 2 hours and became more severe by 48 hours. Vascular alterations, which were predominantly detected in the ruptured vessel, consisted of endothelial cell corrugation, detachment, crater formation, intimal adhesion of platelets and red blood cells, intimal thrombi, and reendothelialization. When cats were pretreated prior to SAH with an anti-platelet-aggregating agent, OKY-1581, the intimal blood elements and thrombi were clearly reduced, and reendothelialization was not observed. However, endothelial cell changes in the OKY-1581-treated group were very similar to those occurring in the nontreated group. While these results suggest that bioactive substances contained within blood platelets, such as growth factors, serotonin, and norepinephrine, have little effect on producing endothelial cell injury, platelets may be important in the initiation of reendothelialization following vessel injury.

Animals↗
PubMed1988

Induction of differentiation of mouse myeloid leukemia M1 cells by serum of patients with chronic myeloid leukemia.

We examined the capacities of sera from patients with myeloid leukemia to induce differentiation in mouse myeloid leukemic M1 cells. Higher differentiation-inducing activity (D-activity) was detected in sera of patients with chronic myelomonocytic leukemia or chronic myeloid leukemia (CML) than in sera of patients with acute myeloid leukemia and normal volunteers. The D-activity in the sera was lost on heating the sera at 56 degrees for 30 min. The major peak of D-activity on Sephadex G-200 gel filtration had an apparent molecular weight of 160,000. The origin of the D-activity in sera of patients with CML was studied by culturing fractions of peripheral blood cells of patients with D-activity for 3 days and then measuring the ability of the conditioned medium (CM) to induce differentiation of M1 cells. The cells in the myeloblast and promyelocyte fraction differentiated spontaneously into macrophage-like cells during culture for 3 days and the cells in the late granulopoietic cell fraction differentiated into neutrophil-like cells. Higher D-activity was present in CM of cells in the myeloblast and promyelocyte fraction than in CMs of late granulopoietic cell fractions. These results suggest that human leukemic cells produce D-activity for M1 cells during their differentiation into macrophage-like cells.

Animals↗
PubMed1988

Accumulation of intimal platelets in cerebral arteries following experimental subarachnoid hemorrhage in cats.

From 2 hours to 23 days following experimental subarachnoid hemorrhage, the accumulation of indium-111-labeled platelets on the intimal surface of the middle cerebral artery was studied in 23 cats. Subarachnoid hemorrhage was produced by transorbital rupture of the right middle cerebral artery. Of the 23 cats, 17 exhibited right middle cerebral artery/left middle cerebral artery radioactivity ratios of greater than 1.25. When these results were compared with those of 12 control cats, 0.001 less than p less than 0.005 (chi2 test). Thus, the results from the control and experimental groups are significantly different and indicate early (after 2 hours) preferential accumulation of intimal platelets in the ruptured right middle cerebral artery compared with the unruptured left middle cerebral artery and new platelet deposition continuing for up to 23 days. However, the experimental group did not reveal a clear pattern for platelet accumulation following subarachnoid hemorrhage. There was no simple correlation between the magnitude of the radioactivity ratios and the time after hemorrhage when the cats were killed although the ratios for 2 hours to 7 days seemed greater than those for 8 to 23 days. Assuming the pivotal role of platelets in the angiopathy of subarachnoid hemorrhage, the administration of antiplatelet agents as soon as possible following its occurrence may be of value.

Animals↗