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Biomedical subjects

E Ito

Publications and source records attributed to E Ito.

At least 163 records · Page 9Linked to original sources
PubMed1995

Expression of erythroid-specific genes in acute megakaryoblastic leukaemia and transient myeloproliferative disorder in Down's syndrome.

Acute megakaryoblastic leukaemia (M7) and transient myeloproliferative disorder in Down's syndrome (TMD) are characterized by rapid growth of abnormal blast cells which express megakaryocytic markers. To clarify properties of the blast cells in M7 and TMD cases, we examined erythroid markers expression in blasts from six cases with M7 and seven cases with TMD in this study. Erythroid-specific mRNAs encoding gamma-globin and erythroid delta-aminolevulinate synthase were found to be expressed in blasts from most of these cases, indicating that majorities of the blasts in M7 and TMD cases have erythroid and megakaryocytic phenotypes. We also found that mRNAs encoding GATA-1 and GATA-2 are expressed in all these cases. These results suggest that M7 blasts and TMD blasts correspond to the erythroid/megakaryocytic bipotential progenitor cells.

5-Aminolevulinate Synthetase↗
PubMed1995

[Is CA125 useful in the management of recurrence of endometrial carcinoma?].

It has been considered that there is no useful serum tumor marker to diagnose endometrial cancer. But recently several reports describe how the serum CA125 value decreases in patients who have received bilateral oophorectomy and in postmenopausal women. In this study, we therefore determined a new cutoff level for serum CA125 and examined the usefulness of serum CA125 in the assessment of recurrence in 42 endometrial cancer cases. These cases were divided into 3 groups: one of 22 low risk cases, 10 moderate risk cases and 10 high risk cases cased by prognosis 1) In the low risk group, 5 cases had a higher serum CA125 level within 1 month after operation than before. 2) In 151 measurements, the mean CA125 value was 9.7 +/- 3.6U/ml, so we considered that 17 U/ml is the cutoff value for determining recurrence. 3) In the low risk group, the CA125 value was either lower than 17U/ml or it has not continued to increase. 4) We divided the high risk group into 3 subgroups into those who had died within 6 months, those who died within 13-14 months and those who died 2-5 years after the initial treatment. In the group who died 13-14 months after the initial treatment, the seurm CA125 level had continued to be high and there was no change in the value after the initial treatment. In the group who died 2-5 years after the initial treatment, the mean +/- S.D. for serum CA125 was 157.3 +/- 158.3U/ml, the maximum was 377U/ml and the minimum was 28U/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1994

Intracellular Ca2+ concentration change of T24 cell under irradiation in the presence of TiO2 ultrafine particles.

We reported that malignant cells are inactivated by photo-excited TiO2 particles (Cai, R.-X., et al. (1992) Cancer Res. 52, 2346-2348). In the present study, the process of cell death of a human bladder cell line T24 with the irradiated TiO2 was investigated by monitoring the time course change in intracellular calcium concentration ([Ca2+]i) under UV irradiation using calcium fluorescence indicator, fura-2. In the presence of photo-excited TiO2 particles (100 micrograms/ml), [Ca2+]i showed a rapid two-step increase; while in the absence of TiO2, it exhibited only a slight and monotonous increase or maintained a constant level. The rapid elevation of [Ca2+]i in the presence of photo-excited TiO2 particles was caused by the influx of extracellular Ca2+ through the plasma membrane and cell death occurred only after the second rapid elevation of [Ca2+]i. These results suggested that the cell membrane permeability to Ca2+ was promoted prior to cell death.

Calcium↗
PubMed1994

Soluble beta-amyloid induction of Alzheimer's phenotype for human fibroblast K+ channels.

Although beta-amyloid is the main constituent of neurite plaques and may play a role in the pathophysiology of Alzheimer's disease, mechanisms by which soluble beta-amyloid might produce early symptoms such as memory loss before diffuse plaque deposition have not been implicated. Treatment of fibroblasts with beta-amyloid (10 nM) induced the same potassium channel dysfunction previously shown to occur specifically in fibroblasts from patients with Alzheimer's disease--namely, the absence of a 113-picosiemen potassium channel. A tetraethylammonium-induced increase of intracellular concentrations of calcium, [Ca2+]i, a response that depends on functional 113-picosiemen potassium channels, was also eliminated or markedly reduced by 10 nM beta-amyloid. Increased [Ca2+]i induced by high concentrations of extracellular potassium and 166-picosiemen potassium channels were unaffected by 10 nM beta-amyloid. In Alzheimer's disease, then, beta-amyloid might alter potassium channels and thus impair neuronal function to produce symptoms such as memory loss by a means other than plaque formation.

Alzheimer Disease↗
PubMed1994

Pentobarbital sodium inhibits the release of noradrenaline in the medial preoptic area in the rat.

The effect of pentobarbital sodium (PB) on noradrenaline (NA) release in the medial preoptic area was studied in ovariectomized rats by a microdialysis method coupled to HPLC. Dialyzates were collected at 6-min intervals before and after the injection in freely moving rats. PB injected i.p. at a dose of 35 mg/kg caused a marked, approximately 40-50% decrease in NA release, which became evident 50 min after the injection and lasted for another 60 min during which the observation was performed. The results suggest that the anesthetic effect of barbiturates is related to the reduction in NA release in the brain.

Animals↗
PubMed1994

Internal Ca2+ mobilization is altered in fibroblasts from patients with Alzheimer disease.

The recent demonstration of K+ channel dysfunction in fibroblasts from Alzheimer disease (AD) patients and past observations of Ca(2+)-mediated K+ channel modulation during memory storage suggested that AD, which is characterized by memory loss and other cognitive deficits, might also involve dysfunction of intracellular Ca2+ mobilization. Bombesin-induced Ca2+ release, which is inositol trisphosphate-mediated, is shown here to be greatly enhanced in AD fibroblasts compared with fibroblasts from control groups. Bradykinin, another activator of phospholipase C, elicits similar enhancement of Ca2+ signaling in AD fibroblasts. By contrast, thapsigargin, an agent that releases Ca2+ by direct action on the endoplasmic reticulum, produced no differences in Ca2+ increase between AD and control fibroblasts. Depolarization-induced Ca2+ influx data previously demonstrated the absence of between-group differences of Ca2+ pumping and/or buffering. There was no correlation between the number of passages in tissue culture and the observed Ca2+ responses. Furthermore, cells of all groups were seeded and analyzed at the same densities. Radioligand binding experiments indicated that the number and affinity of bombesin receptors cannot explain the observed differences. These and previous observations suggest that the differences in bombesin and bradykinin responses in fibroblasts and perhaps other cell types are likely to be due to alteration of inositol trisphosphate-mediated release of intracellular Ca2+.

Adult↗
PubMed1994

Agonist-induced rise in intracellular calcium of lens epithelial cells: effects on the actin cytoskeleton.

Primary cultures of rabbit and skate lens epithelia were used to investigate the effect of calcium release from intracellular stores upon the actin cytoskeleton. Primary cultures were loaded with fura-2 AM and intracellular calcium, i.e. (Ca2+)i, quantitated using a Hamamatsu Photonics digital imaging system. Agonists used were bombesin, inositol-1,4,5-trisphosphate (IP3), thapsigargin (Tg), neuropeptide Y (NPY) and calcium chloride. Recordings were typically made on seven cells in each case. We found that IP3 caused a 6-8-fold immediate release of (Ca2+)i in rabbit cells, but skate cells showed no response unless permeabilized with saponin, whereupon an increase of about 50% occurred. Tg induced release from internal stores in rabbit cells, but had no effect on skate cells. Bombesin caused a large increase in (Ca2+)i release in both, while NPY had no effect in either. Skate cells incubated in calcium-free EGTA-Ringer's solution responded rapidly to addition of 5 mM CaCl2, whereas only three of 35 rabbit cells responded, and in gradual fashion. After calcium imaging, the cells were fixed and stained with rhodamine phalloidin or with an antibody against IP3 receptor (IP3R) conjugated to FITC. Fluorescence microscopy revealed that the actin cytoskeleton had reorganized from the normal stress fiber pattern into polygonal networks. Tg caused the same structures to form in rabbit cells, but bombesin had no effect. IP3 receptor was located intracellularly, presumably on endoplasmic reticulum, and was not associated with plasma membranes. The rapid response of rabbit cells may have been caused by the DMSO in which fura-2 was dissolved. We have found an interesting difference in agonist-induced calcium release between rabbit and skate cells. The latter may utilize either a Ca-Na exchanger or capacitative calcium entry, which could reflect a difference in lens accommodative mechanisms. This seems relevant in view of the fact that the rabbit lens accommodates through change in shape, whereas the skate lens does so through translation of position.

Accommodation, Ocular↗
PubMed1994

Electron microscopic studies on experimental poisoning in mice induced by cylindrospermopsin isolated from blue-green alga Umezakia natans.

The effects of cylindrospermopsin isolated from a blue-green alga Umezakia natans on mice were examined morphologically and biochemically. The main target of the phycotoxin was the liver. The thymus, kidneys and heart were also affected. There were four consecutive phases of the pathological changes in the liver. The initial phase was that of inhibition of the protein synthesis, the second phase of membrane proliferation followed, and then the third phase of fat droplet accumulation and finally the phase of cell death. Using globin synthesis in the rabbit reticulocytes system, it was clearly demonstrated that cylindrospermopsin is a potent inhibitor of the protein synthesis. Protein in microsomes from the mouse livers treated by cylindrospermopsin decreased in amount more significantly than that of phospholipid in microsomes. Furthermore, the amount of total P450 was extensively diminished in the toxin treated with hepatic microsomes.

Alkaloids↗
PubMed1994

Effect of serotonin and tricyclic antidepressants on intracellular calcium concentrations in Spisula oocytes.

Microspectrofluorometry and video imaging techniques were used to study and to compare the changes in intracellular calcium concentrations ([Ca2+]i) of individual Fura-2 loaded Spisula oocytes treated with serotonin (5-hydroxytryptamine, 5-HT) or tricyclic antidepressants. In the present study, we showed that 5-HT increased [Ca2+]i in freshly isolated Spisula oocytes suspended in artificial sea water. In the absence of extracellular Ca2+, 5-HT did not influence [Ca2+]i. Stimulation of [Ca2+]i by 5-HT was blocked by calcium channel blocker, e.g. verapamil, and by tricyclic antidepressants. These observations combined with our previous results on the effects of 5-HT, tricyclic antidepressants and verapamil on calcium uptake suggest that the increase in [Ca2+]i induced by 5-HT results from an influx of extracellular calcium through calcium channels, which can be blocked by tricyclic antidepressants. The use of the Fura-2 imaging technique allowed single-cell measurements and defined changes induced by 5-HT in [Ca2+]i which is the net result of calcium uptake and release of intracellular calcium from storage sites in individual Spisula oocytes.

Animals↗
PubMed1994

Developmental stage- and spermatogenic cycle-specific expression of transcription factor GATA-1 in mouse Sertoli cells.

GATA-1 is an essential factor for the transcriptional activation of erythroid-specific genes, and is also abundantly expressed in a discrete subset of cells bordering the seminiferous epithelium in tubules of the murine testis. In examining normal and germ-line defective mutant mice, we show here that GATA-1 is expressed only in the Sertoli cell lineage in mouse testis. GATA-1 expression in Sertoli cells is induced concomitantly with the first wave of spermatogenesis, and GATA-1-positive cells are uniformly distributed among all tubules during prepubertal testis development. However, the number of GATA-1-positive cells declines thereafter and were found only in the peripheral zone of seminiferous tubules in stages VII, VIII and IX of spermatogenesis in the adult mouse testis. In contrast, virtually every Sertoli cell in mutant W/Wv, jsd/jsd or cryptorchid mice (all of which lack significant numbers of germ cells) expresses GATA-1, thus showing that the expression of this transcription factor is negatively controlled by the maturing germ cells. These observations suggest that transcription factor GATA-1 is a developmental stage- and spermatogenic cycle-specific regulator of gene expression in Sertoli cells.

Animals↗
PubMed1994

Reducing effect of nadolol on serum levels of free thyroid hormones in hyperthyroidism.

We evaluated the effect of the beta-adrenergic receptor blocking agent nadolol on serum levels of free thyroid hormones in 20 untreated patients with Graves' disease, aged between 17 and 57 years (mean +/- SD, 32.9 +/- 10.5). All the patients were treated with 30 mg of nadolol alone once-daily for 2 weeks, and clinical and laboratory parameters before and after the treatment were compared. Systolic blood pressure was depressed significantly (P < 0.001) from 132.7 +/- 11.1 mmHg to 122.8 +/- 10.9 mmHg. The resting pulse rate was also reduced significantly (from 110.3 +/- 9.2/min to 86.0 +/- 13.2/min, P < 0.001). Serum free thyroxine levels were reduced significantly from 7.1 +/- 3.1 ng/dl to 5.7 +/- 3.6 ng/dl (P < 0.05) and serum free triiodothyronine levels were reduced from 21.9 +/- 5.6 pg/ml to 17.2 +/- 6.9 pg/ml (P < 0.01). In the present study, the beta-adrenergic receptor blocking agent nadolol was newly found to have a reducing effect on serum free thyroxine, as well as free triiodothyronine concentrations.

Adolescent↗
PubMed1994

Injury and recovery process of intestine caused by okadaic acid and related compounds.

The injuries and repair processes in the intestines of mice induced by dinophysistoxin 3 (DTX 3) were compared morphologically to those induced by okadaic acid (OA) and dinophysistoxin 1 (DTX 1). DTX 3 impaired intestinal villi by the oral route only, whereas OA and DTX 1 caused intestinal injury with both oral and intraperitoneal exposures. The character of the lesions caused by the 3 toxins and the recovery processes were highly similar. Within 5 min of dosing, the basal portion of the covering epithelium became homogeneous and peeled from the lamina propria, while the upper portion containing microvilli remained intact. There were two types of villous injury and recovery: 1) When the injuries were limited to the villi, new cells from the crypts moved upward and differentiated into columnar cells. 2) When injuries progressed into the glands of Lieberkuhn, clusters of crypt cells were exposed to the intestinal lumen, and in the most severe case they were completely separated. Villous fusion was often seen in the recovery process of the type 2 cases. Recovery from the injuries was almost completed within 2 days. When mice were pretreated with fusarenon-X, a mycotoxin which injuries undifferentiated crypt cells preferentially, the injury induced by OA to the intestinal crypts was exacerbated and the recovery was delayed.

Administration, Oral↗
PubMed1994

[Neuronal development and apoptosis].

There are several distinct mechanisms of neuronal cell death that occurs during development. Nuclear type of cell death involves cell shrinkage and chromatin condensation both typical of apoptosis. Here in this short review we summarize some recent advances concerning the mechanism of nuclear type of neuronal death in vitro. Particular focus is placed on superior cervical ganglion (SCG) cells and neuronal PC12 cells both undergoing apoptosis when they are deprived of NGF or serum/NGF. With regard to presynaptic regulation of neuronal death/survival in SCG both cholinergic and non-cholinergic innervations have a pivotal role. The former may involve the modulation of intracellular free Ca2+ concentration, while the latter may exert its effect through a cAMP-dependent mechanism. Finally, neuronal death/survival mechanism of cerebellar granule cells is discussed in terms of cerebellum development and synaptogenesis. Physiological implications are also described about fyn knockout mouse in which naturally-occurring neuronal death may be greatly impaired.

Animals↗
PubMed1994

Intracellular calcium signals are enhanced for days after Pavlovian conditioning.

Previous observations have implicated GABA as a neurotransmitter released by the vestibular sensory neurons ("hair cells") of the snail Hermissenda onto visual sensory neurons, the type B cells, whose cell bodies are the sites of biophysical and biochemical changes during and following Pavlovian conditioning. Still other observations demonstrated that light-GABA pairings that simulate stimuli presented during Pavlovian conditioning cause prolonged elevation of intracellular Ca2+ and transformation of GABA-induced synaptic inhibition into excitation. Intracellular Ca2+ signals in response to GABA perfused onto the postsynaptic type B terminal branches are shown here to be prolonged on days after conditioning, but not after control paradigms. These and past results demonstrate two separate sites, i.e., the cell body and the terminal branches, for learning-induced changes after Pavlovian conditioning.

Animals↗
PubMed1994

[Role of arachidonic acid metabolites on development of ischemic cerebral edema in rat middle cerebral artery occlusion].

The products resulting from arachidonic acid metabolism of the both cyclo-oxygenase and lipoxygenase pathways possess strong physiological activities, such as vasoconstriction and the enhancement of vascular permeability. Therefore, it is likely that these metabolites are involved in cerebral circulatory disturbance and the formation of brain edema in cerebral ischemia. It is reported that intracerebral injection of leukotriene B4, C4, and E4 increased blood-brain barrier permeability. Thus, it is suggested that leukotrienes may induce vasogenic cerebral edema. We examined role of the products resulting from arachidonic acid of the cyclo-oxygenase and lipoxygenase pathways on the formation of ischemic cerebral edema in rats with focal cerebral ischemia. Focal cerebral ischemia was induced by the occlusion of right middle cerebral artery. Acyclo-oxygenase inhibitor, indomethacin (4mg/kg), was given intravenously 30 minutes before the occlusion of the middle cerebral artery. Also, azerastine hydrochloride (8mg/kg), which has an inhibitory effect on the production and release of leukotrienes from human neutrophil as well as an antagonistic action on leukotrienes and another inhibitory effect on the production of superoxide anion, was given intravenously 5 minutes prior to occlusion. Concentrations of prostaglandin E2 (PGE2), thromboxane B2 (TxB2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and leukotriene C4 (LTC4) measured by radioimmunoassay. The percent water content of a cerebral hemisphere was determined by the wet-dry weight method. In the occluded hemisphere, PGE2, 6-keto-PGF1 alpha, TxB2 and LTC4 significantly increased at 2, 6, 12 hours respectively, following the MCA occlusion as compared to the control levels.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗