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T Maeno

Publications and source records attributed to T Maeno.

At least 55 records · Page 3Linked to original sources
PubMed1994

Suppression of phagocytosis by adrenocorticotropic hormone in murine peritoneal macrophages.

Phagocytosis of latex beads by peritoneal macrophages was examined by means of flow cytometry (FCM). This assay revealed that adrenocorticotropic hormone (ACTH) suppressed phagocytosis in a dose-dependent manner. ACTH (1-24) was more suppressive than ACTH (1-39). Control phagocytosis was partially suppressed in Ca(2+)-free solution. Phagocytosis was suppressed by ACTH in this solution to the same degree as in the normal solution. Suppression by ACTH was reduced in phosphodiesterase inhibitor-containing solution. These results suggest that (1) ACTH suppresses extracellular Ca(2+)-dependent and -independent phagocytosis, (2) the suppression is not mediated by cAMP and (3) the inhibition of macrophage phagocytosis by ACTH is one of the mechanisms that modulate immune responses in stressful situations.

1-Methyl-3-isobutylxanthine↗
PubMed1994

Effects of vesicular acetylcholine uptake blockers on frequency augmentation-potentiation in frog neuromuscular transmission.

Vesamicol inhibits the vesicular loading of acetylcholine molecules. The effects of vesamicol and similarly acting compounds on neuromuscular transmission in frogs were investigated to determine whether these inhibitors-inhibit the frequency augmentation-potentiation of transmitter release. Various vesicular acetylcholine transport blockers suppressed the stimulation frequency-related release parameter, k, in a dose-dependent manner. Artane, cetiedil, chloroquine, ethodin, quinacrine, vesamicol and its benzyl-analogue, 2-(4-benzylpiperidino)cyclohexanol, had strong effects, while those of aminacrine, chlorpromazine, fluphenazine, imipramine, pyrilamine and thioridazine were weak. A significant correlation was observed between the biochemically reported values of IC50 and the electrophysiological inhibitory potencies on k at 20 microM. Contrary to expectations from the biochemical data, however, vesamicol and its benzyl-analogue showed equipotent inhibitory actions on the electrophysiological frequency augmentation-potentiation relation. Low sensitivity and low selectivity of the frequency augmentation-potentiation for vesamicol and its benzyl-analogue lead us to conclude that the vesicular acetylcholine transporter is not the site of the electrophysiological action of vesamicol and similarly acting chemicals.

Acetylcholine↗
PubMed1994

Chemical modification of vesamicol binding sites and frequency augmentation-potentiation in neuromuscular transmission.

Vesamicol (AH5183), a potent and specific inhibitor of the vesicular acetylcholine uptake system, reduces at relatively high doses the slope of the log-linear frequency augmentation-potentiation (FAP) relation observed between the mean quantal content of endplate potential and the stimulation frequency. Recent biochemical studies identified two binding sites for vesamicol; one is the vesicular acetylcholine uptake system and the other is the vesamicol binding protein localized in the nerve terminal membrane. The present experiments were designed to determine the exact site of action of vesamicol on the FAP relation. Studies using epsilon-maleimidocaproic acid and picrylsulfonic acid, both membrane-impermeant protein-modifying reagents, revealed that these reagents diminished the vesamicol effect concomitant with an impairment of the functioning site for FAP. Because of the membrane-impermeant nature of the reagents, the present results were interpreted to mean that a vesamicol binding protein or a related component, localized in the nerve terminal membrane, is the target of action by vesamicol. This vesamicol binding component seems to play an important role in the stimulation frequency-dependent modulation of the evoked release of transmitter quanta observable as FAP.

Animals↗
PubMed1994

Analysis of intra- and intercellular calcium signaling in a mouse malignant glioma cell line.

Intra- and intercellular calcium signaling in glioma cells was examined by mechanical stimulation of a monolayer cell line of methylcholanthrene-induced mouse ependymoblastoma, 203-glioma, with a fine round-tip glass needle. A fura-2 fluorescence image of the glioma revealed a four- to eightfold increase in the cytosolic calcium ion concentration in directly stimulated signal cells. The increased calcium spread to surrounding cells at a speed of 20 microns/sec for a distance of up to 200 microns. Calcium was transmitted between adjacent cells and even in cells up to 200 microns distant from the initially stimulated cell. Microinjection of Lucifer yellow dye showed no gap junctional communication between cells. Depletion of extracellular calcium ion inhibited both cytosolic calcium elevation and propagation to neighboring cells by mechanical stimulus. An intracellular calcium blocker, TMB-8, eliminated the cytosolic calcium mobilization in a mechanically stimulated cell, but had no effect on calcium diffusion to surrounding cells. Nifedipine and verapamil, antagonists of voltage-dependent calcium channels, did not act on the mechanically induced calcium response. This suggests that some stimulating factor may trigger transmission of calcium, which may be ejected directly from single stimulated cells and mediated via a membrane receptor but not through a gap junction. The calcium signaling in a mechanically stimulated cell may be related to both an influx and a redistribution of intracellular calcium from internal stores, while calcium propagation to neighboring cells may involve calcium influx alone.

Animals↗
PubMed1994

[Effectiveness of thrice-weekly injection of romurutide for prophylaxis of leukocytopenia during radiation therapy].

The effectiveness of thrice-weekly injection of Romurutide for leukocytopenia due to radiation therapy was analyzed. Twenty-two patients were randomly divided into two groups. Ten of group A cases were injected 3 times per week 10 times (3 weeks) and 12 of group B cases were injected 5 times per week 10 times (2 weeks). White blood cell counts and neutrophil numbers in group A were almost the same as in group B at day-3 and day-8, and those in group A were more than in group B at day-15 and day-22, although there were no statistical significances. Lymphocyte percentages, monocyte percentages and platelet cell counts between groups showed no differences. Injections were stopped in 3 cases due to fever (2 in group A, 1 in group B). The effects were recognized in nineteen cases (excluding above 3 cases). The effect of this thrice-weekly injection method during the injection period was the same or more than with 5 injections/week, and the period of the former was 50% longer. The 3 weekly injection method is more effective for prophylaxis of leukocytopenia.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1994

[Growth of the hypoplastic aortic arch after arch repair for coarctation and interruption of the aorta].

Surgical treatment for a hypoplastic aortic arch associated with coarctation or interruption of the aorta is controversial. We evaluate the changes of diameter of proximal transverse aortic arch after surgery in 28 patients. Proximal transverse aortic arch in all patients was preoperatively 3.5 +/- 0.9 mm (2.5 to 7 mm), and 54 +/- 12% (36 to 84%) to the normal aortic valve dimension (n-AVD: 16.6 X BSA0.6). While postoperative proximal transverse aortic arch was 6.5 +/- 1.8 mm, and 76 +/- 12% to the n-AVD, and significantly grew more than the preoperative arch dimension (p = 0.0001). In 18 patients having two times cardiac catheterization postoperatively, proximal transverse aortic arch was 6.5 +/- 1.6 mm, and 75 +/- 13% to n-AVD on the 1st postoperative examination. On the 2nd examination, the arch was 9.9 +/- 1.9 mm, and 88 +/- 12% to n-AVD, and significantly grew with increasing years (p < or = 0.0003). We concluded that the proximal transverse aortic arch, which was more than 36% to n-AVD in diameter, if not dilated surgically, grew with increasing years after aortic arch repair.

Aorta, Thoracic↗
PubMed1994

[Subaortic stenosis in coarctation or interruption of the aorta--changes of left ventricular outflow tract dimension after aortic arch repair and pulmonary artery banding].

Left ventricular outflow tract (LVOT) dimension was measured in seven patients with coarctation (CoA) or interruption (IAA) of the aorta before and after aortic arch repair and pulmonary artery banding. The age of patients ranged 3 to 69 (mean 16) days, the weight 3.0 to 3.9 (mean 3.4) kg. Associated cardiac anomalies were VSD in 6, MA and DORV in 1. In five patients compared by ultrasound, preoperative LVOT dimension ranged from 3.5 to 5.0 (mean 4.4) mm with the ratio to the normal aortic valve dimension (n-AVD; 16.6 x BSA0.6) from 54 to 82 (mean 69)%. Postoperative dimension increased 5.0 to 7.4 (mean 5.7) mm and the ratio to the n-AVD increased 65 to 89 (mean 80)%. In three patients compared by LV graphy, preoperative LVOT dimension ranged from 4.0 to 4.5 (4.2) mm and the ratio ranged from 61 to 72 (68)%. Postoperative dimension increased from 4.5 to 6.7 (5.3) mm, and 74 to 80 (78)% to n-AVD after operation. Postoperative pressure gradients between LV and ascending aorta in each patient were 1 to 9 (mean 6) mmHg. In any patients, LVOT obstruction did not advance after aortic arch repair and pulmonary artery banding.

Aorta↗
PubMed1994

[Effects of nilvadipine on membrane potential in cultured neuroblastoma-glioma hybrid NG108-15 cells].

Examination was made of the effects of nilvadipine on membrane potential in cultured neuroblastoma-glioma hybrid NG108-15 cells using the current clamp method. The NG108-15 cells line differentiates into neuronal cells following the addition of 1mM dibutyryl cAMP to the culture medium. This agent (nilvadipine) was found to inhibit both sodium and calcium current on the cell membranes of differentiated NG108-15 cells. The inhibitory effect was reversible in a dose-dependent manner between 10 and 100 microM. A substantial washing-time with normal saline, over 20 minutes, was needed for complete recovery from inhibition. The higher the concentration of nilvadipine, the more suppressive was the action on the membrane potential. A higher dose of nilvadipine, 100 microM, caused the disappearance of the peak membrane potential. This effect appeared irreversible, when cells were incubated in the presence of 100 microM nilvadipine for a longer time. Nilvadipine may thus exert inhibitory effect on the electrophysiological activity of neuronal cells, especially the calcium current of the membrane.

Animals↗
PubMed1993

[Results of electron beam irradiation for tongue cancer].

One hundred and eighty three patients with squamous-cell carcinoma of the tongue were treated with electron beam irradiation at the Dept. of Radiology, Nihon University School of Medicine, from 1967 to 1988. We analyzed the therapeutic results of the investigation to find out indications of squamous-cell carcinoma of the tongue to see if it could be treated by intra-oral cone irradiation with electron beam (IOC). The patients were restaged, as follows: stage I, 38 cases: stage II, 64 cases: stage III, 58 cases: stage IV, 23 cases. There were 113 males and 70 females, ranging in age from 18 to 87 years old. IOC was applied for T 1 or smaller T 2 cases. External neck irradiation and IOC were combined for larger T 2, T 3 or T 4 cases. The two-year local-control rates for primary lesions with the present method were 85% for T 1, 73% for T 2, and 58% for T 3. There were no two-year local-control cases for T 4. Clinical feature of the tumor were classified into tumourous type, small ulcerating type, and large ulcerating type. The two-year local-control rates were as follows: 80% for tumorous types, 68% for small ulcerating types and 53% for large ulcerating types. Uneven fractionated irradiation was performed on 144 cases and even fractionated irradiation was performed on 39 cases. The two-year local-control rates were as follows: 68% for uneven fractionated irradiation cases, 61% for even fractionated irradiation. In T 2 and T 3 cases, the two-year local-control rates were as follows: 77%, 63% for uneven fractionated irradiation cases, 56%, 40% for even fractionated irradiation cases. The two-year local-control rates were increased by uneven fractionated irradiation for T 2, T 3 cases (P < 0.05). We analyzed the therapeutic results in details for T 3 cases. T 3 patients were classified into two categories according to tumor size (category 1: long axis X short axis > 1000mm2: category 2: long axis X short axis < or = 1000mm2). The two-year local-control rates were 48% for category 1, and 72% for category 2. T 3 patients were classified into two categories according to clinical feature of the tumor (tumors with ulcers and tumors without ulcers). The two-year local-control rates were 43% with ulcers, and 74% without ulcers. The actuarial five-year survival rates were 92% for stage I, 72% for stage II, 67% for stage III, and 12% for stage IV.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1993

Proliferation-associated increase in sensitivity of mammary epithelial cells to inositol-1,4,5-trisphosphate.

Injection of D-myo-inositol-1,4,5-trisphosphate (IP3) was found to induce a transient increase of intracellular Ca2+ concentration in cancerous mammary cells (MMT060562) and in normal mammary cells treated with epidermal growth factor. Responses to injection of either D-myo-inositol-1,4-bisphosphate (IP2) or D-myo-inositol-1,3,4,5-tetrakisphosphate (IP4) were small or absent. Furthermore, normal mammary cells cultivated with low-protein serum replacement alone or in the presence of differentiation-inducing hormones (insulin + cortisol + prolactin) were less sensitive to IP3. Thapsigargin induced a transient increase of Ca2+ due to the release of Ca2+ from an intracellular pool. There was no difference in the peak heights of the thapsigargin-induced Ca2+ increase when mammary cells were cultivated in the presence or absence of epidermal growth factor or insulin + cortisol + prolactin. These findings suggest that the releasable intracellular Ca2+ pool remained unchanged whereas sensitivity to IP3 increases during the proliferation stage. Mechanical stimulus of a mammary cell induces an increase of intracellular Ca2+ in the stimulated cell. A certain stimulating factor is released from the mechanically stimulated cell into the extracellular space, and it induces an increase of Ca2+ in surrounding cells. In contrast, the IP3-induced Ca2+ increase in both cancerous and epidermal growth factor-treated normal mammary cells did not spread to adjacent cells. Therefore, increase of Ca2+ is not sufficient to account for the release of stimulating substances from mammary cells in the mechanically-induced spreading response.

Animals↗
PubMed1993

Inositol 1,4,5-trisphosphate mediates adrenaline activation of K+ conductance in mouse peritoneal macrophages.

In mouse peritoneal macrophages, alpha 1-adrenoceptor stimulation evokes a Ca(2+)-dependent K+ current [Io(Adr)][Hara et al. (1991) Pflügers Arch 419:371-379]. The roles of D-myo-inositol 1,4,5-trisphosphate (InsP3) and a GTP-binding protein (G protein) in Io(Adr) were investigated with tight-seal whole-cell recordings and fura-2 fluorescence measurements. Intracellular injection of InsP3 (5-50 microM) evoked transient outward currents [Io(InsP3)] with or without damped oscillations in membrane currents at -40 mV. Dialysis with 0.2 mM guanosine 5'-[3-thio]triphosphate (GTP[gamma S], a poorly hydrolysable GTP analogue) at -40 mV activated oscillatory outward currents or a slowly developing steady current on which such oscillations were superimposed after a delay of 10-90 s. Io(InsP3) and the GTP[gamma S]-induced current [Io(GTP[gamma S])] were accompanied by an increase in conductance. Reversal potentials of both responses closely depended on the extracellular K+ concentration. Fura-2 measurements revealed that Io(InsP3) and Io(GTP[gamma S]) result from a rise in intracellular free Ca2+ concentration ([Ca2+]i). Removal of extracellular Ca2+ did not abolish Io(InsP3) and Io(GTP[gamma S]). Both were blocked by bath-applied charybdotoxin. Intracellular D-myo-inositol 1,3,4,5-tetrakisphosphate (InsP4, 50 microM) did not evoke any responses, whereas D-myo-inositol 2,4,5-trisphosphate [InsP3(2,4,5), 20 microM] elicited an outward current at -40 mV. Io(InsP3) was completely blocked by prior dialysis with the InsP3 receptor antagonist heparin (5 mg/ml). Inclusion of guanosine 5'-[2-thiol] diphosphate (GDP[beta S], 2 mM) or heparin (5 mg/ml) together with GTP[gamma S] in the patch pipette solution completely blocked Io(GTP[gamma S]). These results indicate that intracellular injection of InsP3 or GTP[gamma S] mimic Io(Adr).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

The alpha 1A-adrenoceptor couples to Ca2+ mobilization in mouse peritoneal macrophages.

Activation of the alpha 1-adrenoceptor (alpha 1-AR) in mouse peritoneal macrophages induces a Ca(2+)-dependent K+ current via release of Ca2+ from internal stores [Hara et al. (1991) Pflügers Arch 419: 371-379]. In order to characterize the alpha 1-AR subtype in macrophages, we examined potencies of the alpha 1-AR subtype-selective antagonists against epinephrine-induced increases in intracellular Ca2+ concentration ([Ca2+]i). The Ki values for the alpha 1-AR in macrophages of WB4101, 5-methylurapidil and phentolamine were 0.13 nM, 0.15 nM and 7.0 nM, respectively. (+)-Niguldipine (10 nM) completely blocked the response. Treatment with chloroethylclonidine (CEC) did not abolish the response. These pharmacological properties of the alpha 1-AR in macrophages agree quite well with those of the alpha 1A subtype.

Animals↗
PubMed1993

[The evaluation of interval period to prepare the left ventricle for Jatene operation for simple transposition of the great arteries].

Laboratory studies indicate that it can be as short as one week after a first-stage operation to prepare the left ventricle for a subsequent second-stage arterial switch (Jatene operation) for simple transposition of the great arteries (TGA). In order to ascertain it, we evaluated the left ventricular (LV) function immediately after the first-stage procedure and late postoperatively by echocardiography and catheterization. There were 6 cases with simple TGA. The age at palliation was 6.6 +/- 4.5 (mean +/- SD) months, and the interval between the first-stage and Jatene operation was 16 days-16 months (6.7 +/- 6.4 months). All patients survived after arterial switch. In 2 early infant cases, arterial switch operation was performed with ventilatory support due to cardiac and respiratory failures 16 and 21 days after the first-stage operation respectively. LV end-diastolic dimension increased by 1 week and showed no change after 1 week (n = 4). LV ejection fraction was depressed from 0.84 +/- 0.03 preoperatively to 0.61 +/- 0.08 at 1-4 days after the first-stage operation but improved to 0.83 +/- 0.06 by 7-9 days after that (n = 4). LV end-diastolic posterior wall thickness increased to more than 4 mm in 3 infant cases, more than 3 mm in 2 early infant cases by 7 days. The results of catheterization after the first-stage operation were as follows (n = 5); left ventricular right ventricular peak systolic pressure ratio increased from 0.53 +/- 0.16 to 0.94 +/- 0.04 (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1993

Mechanically induced calcium signal in mammary epithelial cells.

In mouse mammary epithelial cells, mechanical stimulation of a cell induced an increase of intracellular Ca2+ concentration (Ca2+i), which spread from the stimulated cell to the surrounding cells with a conduction velocity of about 10 microns/s. The Ca2+i signal was transmitted between isolated cells or separated colonies, where there was no physical contact between them. The flow of medium changed the spreading pattern of Ca2+ wave. The Ca2+ wave was induced even in Ca(2+)-free solution. These findings suggested that a certain factor was released from stimulated cell to extracellular medium and it induced the Ca2+i increase from intracellular store in the surrounding cells.

Animals↗
PubMed1993

[Effect of enalaprilat, an angiotensin converting enzyme inhibitor, on the membrane potential of cultured neuroblastoma-glioma hybrid NG108-15 cells].

The effect of enalaprilat on the membrane potential of cultured neuroblastoma-glioma hybrid NG108-15 cells was investigated using the current clamp method. The NG108-15 cell line characteristically differentiates into neurons after addition of 1 mM dibutyryl cAMP to the culture medium. First it was found that enalaprilat inhibits both sodium and calcium currents in the cell membrane of differentiated NG108-15 cells. At concentrations between 10 and 100 microM, this inhibitory effect was reversible and transient, and occurred in a dose-dependent manner. Prolonged washing with normal saline (> 20 min) was needed to completely reverse the inhibitory effect of enalaprilat. The higher the concentration of enalaprilat, the greater its suppressant action on the membrane potential, and at high concentrations (100 microM), enalaprilat caused the peak membrane potential to disappear. When cells were incubated with enalaprilat, 100 microM, for longer periods, however, this inhibitory effect appeared to become irreversible. These findings suggest that enalaprilat has an inhibitory effect on the electrophysiological activity of neurons especially on membrane calcium currents.

Animals↗
PubMed1992

The neuropeptide, neuromedin C, activates a potassium current in mouse macrophages.

Neuromedin C (NmC) induced an outward current (Io(NmC)) in macrophages. Reversal potentials were dependent on external K+ concentrations ([K+]o) and independent of [Cl-]o. Tetraethylammonium (TEA) and quinidine effectively suppressed Io(NmC). Charybdotoxin (ChTX) and apamin had little effect. Io(NmC) was abolished in Ca(2+)-free EGTA-containing solution. These results suggest that MnC activates a Ca(2+)-dependent K+ current (IK,Ca) and can modulate activities in macrophages.

Amino Acid Sequence↗
PubMed1992

Induction of two K+ currents by complement component C5a in mouse macrophages.

Puff application of complement component C5a (5 x 10(-8) M) onto peritoneal macrophages from thioglycollate-stimulated mice induced two kinds of outward current at a holding potential of -68 mV, a slowly-rising sustained outward current and a spike-like transient outward current. Quinidine (2 x 10(-4) M) and tetraethylammonium (10(-2) M) partially suppressed both types of outward current. Charybdotoxin (2 x 10(-6) M) markedly suppressed the spike-like outward current. Reversal potentials in bath solutions of different external K+ concentrations were dependent only on K+ concentrations. The transient current was not suppressed in Ca(2+)-free EGTA-containing solution, but was completely abolished in BAPTA-containing solution. One kind of single channel responding to C5a, which has a single-channel conductance of 29 pS, was recorded from cell-attached patches. These results suggest that C5a activates a Ca(2+)-dependent and another type of K+ current.

Animals↗