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Y Honma

Publications and source records attributed to Y Honma.

At least 289 records · Page 16Linked to original sources

[The role of brain-stem vasomotor centers on the neurogenic control of cerebrovascular tonus. Part 2: The effect of stimulation of the medullary reticular formation on cerebrovascular tonus].

Acute brain swelling has been proposed to be caused by vasomotor paralysis secondary to disruption of metabolic and/or neurogenic control of cerebrovascular tone. In previous experiments, acute brain swelling was produced by stimulation of the reticular formation of the medulla oblongata (MORF) with destruction of the dorsomedial nucleus of the hypothalamus (DM) and the reticular formation of the midbrain (MBRF) in 2 (out of 56) animals. The purpose of the present study is to clarify the effect of stimulation of the MORF on cerebrovascular tone. Using 32 cats, blood pressure (BP), intracranial pressure (ICP) and cerebral blood volume (CBV) were continuously measured. The animals were divided into 4 groups: those in which the ICP was normal (Group A), those in which the ICP increased after subarachnoid hemorrhage (Group B), those which underwent superior cervical ganglionectomy (Group C) and those in which the spinal cord was transected at the C2 level (Group D). In all animals, the MORF was stimulated after the DM and MBRF were destroyed. Thirty minutes after cessation of stimulation, the BP was increased again by injection of angiotensin II until it reached the same level as with MORF stimulation. The vasomotor index (VI), defined by delta ICP/delta BP, was calculated and compared between the two situations. BP, ICP and CBV increased simultaneously immediately after MORF stimulation. In 29 out of the 32 animals, ICP increased abruptly from 2 to 48 mmHg and after ten seconds or more decreased gradually. The BP rose about 50 mmHg more slowly than the ICP. After cessation of MORF stimulation, BP, ICP and CBV returned to the control value.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

[The effect of brain-stem vasomotor centers on the neurogenic control of cerebrovascular tonus--Part 3. The effects of destruction and stimulation of the brain-stem on intracranial pressure in acute subarachnoid hemorrhage].

The purpose of the present study is to clarify the effects of destruction and stimulation of the brain-stem on intracranial pressure (ICP) in experimentally induced subarachnoid hemorrhage (SAH). Using 23 cats, blood pressure (BP), ICP and local cerebral blood volume (CBV) were continuously measured. Acute SAH was produced by injection of autogenous blood (3 to 7 ml) into the cisterna magna. The animals were divided into two groups. Group A: those in which hypothalamic dorsomedial nucleus (DM) and reticular formation of the midbrain (MBRF) were coagulated bilaterally one hour after SAH and Group B: in addition to the procedure of Group A, reticular formation of the medulla oblongata (MORF) was electrically stimulated bilaterally. In 19 out of 23 cats of both groups, transient small increases in ICP and CBV were observed during coagulation and/or stimulation of DM, MBRF and MORF respectively in the animals whose ICP remained approximately 20 mmHg or below and progressive increase in ICP was never evoked. In 3 animals of Group A whose ICPs remained high at more than 20 mmHg, sequential destruction of DM and MBRF induced stepwise increase in ICP to 40 to 80 mmHg and consequently resulted in acute brain swelling. In 1 animal of Group B whose ICP fluctuated around 20 to 40 mmHg, biphasic increase in ICP to 100 mmHg was repeatedly evoked by stimulation of MORF. It is concluded that in the condition of increased ICP produced by SAH, lesions in the DM and MBRF and stimulating condition of MBRF may result in acute brain swelling.

Acute Disease↗

Specific inhibition by prostaglandin D2 and its metabolites of lysozyme synthesis in mouse macrophage-like cell line, Mm-1.

The cultured mouse macrophage-like cell line Mm-1 synthesizes and secretes lysozyme continuously like normal macrophages. Culture of the cells in the presence of prostaglandin D2 for 3 days strongly inhibited their production of lysozyme activity. Prostaglandin D2 caused dose-dependent inhibition of the activity: 1 X 10(-6) M prostaglandin D2 caused about 50% inhibition. Inhibition by prostaglandin D2 was not related to cytotoxicity and was reversible. The rate of synthesis of lysozyme protein was measured by culturing Mm-1 cells with radioactive amino acids and then immunoprecipitating the protein. At the concentrations used, prostaglandin D2 inhibited the synthesis of lysozyme dose-dependently, but did not suppress the synthesis of total protein. Of the various types of prostaglandin, only prostaglandin D2 inhibited the production of lysozyme in Mm-1 cells. Moreover, prostaglandin D2 did not inhibit the production of other lysosomal enzymes, such as acid proteinase, acid phosphatase and beta-glucuronidase, and did not affect Fc receptors on the cell surface, adherence of cells to the culture dish or the cell morphology. These results indicate that prostaglandin D2 specifically inhibits the synthesis of lysozyme in Mm-1 cells. When Mm-1 cells were cultured for 3 days in the presence of the ethyl acetate extract from the culture medium in which Mm-1 cells had been cultured with prostaglandin D2 for 3 days, the production of lysozyme activity of Mm-1 cells was also markedly inhibited by the extract. After the incubation of prostaglandin D2 for 3 days with Mm-1 cells, less than 10% of the initial prostaglandin D2 remained and two major metabolites appeared. These results suggest that the metabolites of prostaglandin D2 were involved in the inhibitory action of prostaglandin D2 in Mm-1 cells.

Animals↗

Discrepancy between in-vitro and in-vivo inductions of differentiation by retinoids of human acute promyelocytic leukemia cells in relapse.

In-vitro studies of leukemic cells with retinoic acid and a therapeutic clinical trial with its derivative, etretinate, in a 58 yr-old male patient with 15;17 translocation-positive acute promyelocytic leukemia (APL) in relapse are reported. Actinomycin D was used in combination. Bone marrow promyelocytes from the patient prior to etretinate and actinomycin D matured morphologically in the liquid culture with retinoic acid; 98% were matured myeloid cells after 6 days at a concentration of 10(-6) M of retinoic acid as compared with 2% in the control culture. Positive NBT reactions were seen in none of the cells in the latter but in 95% of the cells in the former. Actinomycin D, when added alone, only induced NBT positivity, but, when used in combination with retinoic acid, increased both NBT positivity and morphologically matured cells. The patient was treated daily with 2 micrograms/kg of actinomycin D (or 20 mg/m2 or 33 mg/m2 cytosine arabinoside after the 6th day) in 24-h infusions and per oral 90 mg/body of etretinate. No effectiveness was observed both morphologically and clinically. The patient expired 15 days after the initiation of etretinate. Thus, a discrepancy existed in the response of leukemic cells from this relapsed patient with APL to the in-vitro and in-vivo attempts to include differentiation by retinoids and actinomycin D.

Cell Differentiation↗

Spindle and giant cell carcinoma of the bladder. Report of 3 cases.

3 cases of spindle and giant cell carcinoma are reported. 2 patients with T3N0M0 and T3N1M0 tumors underwent radical cystectomy. They died 8 and 9 months after cystectomy for local recurrence and tumor metastases. Neither radiotherapy nor chemotherapy were effective in these 2 patients. 1 patient with T1NXM0 disease underwent resection of the tumor through cystotomy. Although she had neither adjuvant chemotherapy nor radiotherapy, she is well without recurrence 6 years after surgery. Early surgical resection of the tumor may be the only currently accepted therapy of spindle and giant cell carcinoma of the bladder.

Aged↗

Characterization of a differentiation-inhibitory activity from 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-activity) has been found in conditioned medium of variant M1 cell clones resistant to differentiation inducers, and this I-activity has been shown to be closely associated with resistance of the cells to differentiation inducers. In this work, the I-activity in the conditioned medium of the resistant M1 cells was shown to bind to Carboxymethyl-Sepharose CL-6B and to be eluted with 0.27-0.4 M NaCl. The profile of gel filtration of I-activity from Sephadex G-200 indicated considerable heterogeneity in molecules with I-activity; the apparent molecular range of the main I-activity was 60,000-80,000. On chromatofocusing, the I-activity was eluted with Polybuffer 96-acetic acid at pH 8.8-9.0. The I-activity was inactivated by treatment with trypsin or by heating at 75 degrees C for 30 min. Therefore, the main I-activity seemed to be due to a basic protein(s).

Animals↗

Induction of differentiation of cultured mouse monocytic leukemia cells (Mm-A) by inducers different from those of parent myeloblastic leukemia cells (M1).

Mouse monocytic Mm-A cells are a highly leukemogenic variant line of the monocytic and non-leukemogenic cell line Mm-1, which developed spontaneously from mouse myeloid leukemia M1 cells. Studies were made on whether Mm-A cells could be induced to differentiate further by agents that were effective for inducing differentiation of the parent M1 cells and other leukemic cells. Of the agents tested, butyrate, conditioned medium from concanavalin A-stimulated spleen cells, lipopolysaccharide (LPS) and N6,O2-dibutyryl adenosine 3'5'-cyclic-monophosphate (dbcAMP) significantly stimulated the lysozyme activity of Mm-A cells, which is one of the most characteristic biochemical markers of monocytes and macrophages. Butyrate was the most effective agent for increasing lysozyme production by Mm-A cells; culture with 0.5mM butyrate for 3 days increased lysozyme production by Mm-A cells about 50-fold. Inducers of M1 cell differentiation such as dexamethasone, 1 alpha,25-dihydroxyvitamin D3, arginase, and proteinous inducer did not increase the lysozyme activity. Butyrate also induced NBT reduction and stimulated other differentiation-associated functions, such as expressions of Fc receptors on the cell surface, immune phagocytosis and production of inducer for M1 cell differentiation. Its effect in stimulating differentiation of Mm-A cells was synergistic with that of dbcAMP or LPS. Incubation with butyrate inhibited the proliferation of Mm-A cells, about 0.3mM butyrate causing 50% inhibition. These results indicate that monocytic, leukemogenic Mm-A cells can be induced to differentiate further by butyrate and that the inducers of differentiation of Mm-A cells are markedly different from those of the parent myeloblastic M1 cells.

Animals↗

[Farmer's lung in the east of Hokkaido--its geographical distribution].

Fourteen cases of farmer's lung, which were clinically and pathologically defined, were reported. The incidence of disease in Hokkaido was estimated to be 1-2% and its geographical distribution was uniform. It was stressed that there is a considerable number of undiagnosed patients with farmer's lung.

Adult↗

Selection of mouse macrophage-like sublines that differ in leukemogenic potential and characterization.

The murine macrophage-like cell line (Mm-1), which is nonleukemogenic to syngeneic SL mice, was originally derived from spontaneously differentiated cells of a clonal line of mouse myeloid leukemia cells (M1). In the present experiment, variant cell lines with a high (Mm-A), moderate (Mm-P), and little or no (Mm-S1 and Mm-S2) leukemogenic potential were obtained from the Mm-1 cells. The mean survival times of syngeneic SL mice inoculated i.p. with 5 X 10(6) Mm-A and Mm-P cells were 17 and 33 days, respectively, whereas almost all the mice inoculated with Mm-S1 or Mm-S2 cells survived for more than 90 days. These variant cell lines did not lose their macrophage-like characteristics in vitro. These variant cell lines phagocytized latex beads and sensitized sheep erythrocytes, produced lysozyme, and adhered to culture dishes. The four variant cell lines showed no significant difference in proliferation rates in vitro in liquid medium containing 10% calf serum, but Mm-A cells could grow both in soft agar medium in the absence of ascitic fluid containing colony-stimulating factor (CSF) and in liquid medium containing 1% serum, whereas Mm-P cells could grow in the liquid medium but not in soft agar medium without ascitic fluid, and Mm-S1 and Mm-S2 cells could not grow in either medium. The ratio of the nuclear area to the cell area (NCR) of Mm-A cells was a high (51%) but those of Mm-S1 and Mm-S2 cells were low (40-41%), and that of Mm-P cells was intermediate (44%). The leukemogenicity of Mm-1 cell lines was roughly correlated with their NCR. The possibility that interactions between Mm-1 variant cells and host immune cells might be involved in the mechanisms of their different leukemogenicities was not supported by results on the in vitro susceptibilities of Mm-1 variant cells to the cytostatic actions by normal macrophages and spleen cells and on leukemogenicities of the Mm-1 variant cells in athymic nude mice. A possible method of control of the leukemogenicity of Mm-1 variant cells is discussed.

Animals↗

Antiallergic agents. 3. N-(1H-tetrazol-5-yl)-2-pyridinecarboxamides.

A series of N-tetrazolylpyridinecarboxamides was prepared and evaluated for antiallergic activity by the passive cutaneous anaphylaxis (PCA) assay. From the structure-activity relationships (SAR) of this class of compounds, it was revealed that the N-tetrazolylcarbamoyl group as an acidic functionality is required to be at the 2-position of the pyridine nucleus and that the phenyl group as a subtituent is not necessarily required for activity. 6-Methyl-N-(1H-tetrazol-5-yl)-2-pyridinecarboxamide (36) showed good oral activity and low toxicity.

Animals↗

Rib cage and abdominal contributions to ventilatory response to CO2 in infants.

We have measured the ventilatory response to inhaled CO2 of six newborn infants in rapid-eye-movement (REM) and non-REM (NREM) sleep. Ventilatory responses were measured using the Read rebreathing technique. The response was further partitioned into the volume contributions of the rib cage and abdominal compartment using the respiratory inductance plethysmograph. Sleep state was defined by electroencephalogram, electrooculogram, and behavioral criteria. In NREM sleep, there was a highly significant linear correlation between both tidal volume (VT) and instantaneous minute ventilation (VI) with CO2. Among infants, the slope of VT varied from 1.0 to 0.34 ml X Torr-1 X kg-1. However, these differences were largely due to differences in rib cage contribution, which varied from 0.56 to -0.08 ml X Torr-1 X kg-1. The abdominal contribution was similar among infants (0.41-0.56 ml X Torr-1 X kg-1). In REM, the slopes of VI were less steep than in NREM, with greater breath-to-breath variability. Slopes of VT also tended to be lower. The abdominal responses were similar to those in NREM, whereas the rib cage response was low and negative in three studies. We conclude that the slope of the CO2 response curve is primarily determined by the extent of rib cage recruitment.

Abdominal Muscles↗