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Biomedical subjects

K Tasaka

Publications and source records attributed to K Tasaka.

At least 181 records · Page 10Linked to original sources
PubMed1989

Complete remission of recurrent glioblastoma multiforme following local infusions of lymphokine activated killer cells. Case report.

We report the case of a 26-year-old man in whom glioblastoma multiforme had recurred six months following a subtotal resection. Despite radiotherapy and a course of interferon beta and ACNU, the tumour increased in size (to 3 cm) and there was neurological deterioration. Treatment was then initiated with LAK cells, together with ACNU and interferon beta. After three courses of LAK cells, tumour size was markedly reduced, and at about six months the tumour had nearly disappeared on computed tomographic (CT) scans. At one year, and after nine courses of LAK cell therapy (total dose of 2.7 x 10(9) cells) infused via an Ommaya reservoir and supplemented by ACNU and interferon beta, the tumour has disappeared and the patient is considered to be in complete remission since 6 months. This marked response is thought to be due chiefly to LAK cell therapy. The relatively low dose administered was well-tolerated.

Adult↗
PubMed1989

Microfilament-associated degranulation of sensitized guinea-pig lung mast cells.

When sensitized guinea-pig lung mast cells were exposed to antigen, granules were pushed out on to the cell surface. Subsequently, thin filaments, some extending as long as 15 microns, were projected radially with the extruded granules. The latter became swollen in the extracellular medium and the elongated filaments became shorter, until, within 7-8 min, the granules were reincorporated into the cytoplasm. The time course of morphological changes corresponded approximately to that of changes in the intracellular Ca2+ concentrations. The filaments connecting the extruded granules to the cell surface were stained with rhodamine-phalloidin, indicating that they consisted mainly of actin.

Actin Cytoskeleton↗
PubMed1989

Excitatory effect of histamine on EEGs of the cortex and thalamus in rats.

When low frequency electrical stimulations were repeatedly applied to the rat midbrain reticular formation, the EEG spectral power recorded at the cortex and thalamus increased markedly, especially in the low frequency bands (0-6 Hz). The intraventricular administration of histamine (Hi) inhibited this increase. Hi-induced inhibition was antagonized by simultaneous injection of an equimolar dose of either pyrilamine or diphenhydramine, but not by that of cimetidine. In accordance with this, 2-methylHi decreased the power in the slow wave region, while 4-methylHi was not effective. It was assumed that the EEG arousal effect of Hi is exerted via H1 receptors but not related to H2 receptors. Adverse effects of H1 blockers on the brain, such as drowsiness, may be produced as a consequence of this inhibitory action.

Animals↗
PubMed1989

Proliferative activity of autoimmune MRL mouse serum IgG to interleukin 3-dependent cell line through autocrine mechanism.

Serum of an autoimmune MRL/Mp-lpr/lpr (MRL/l) mouse supported the proliferation of interleukin 3 (IL-3)-dependent cell line, FDC-P2. This IL-3-like activity initially appeared at 1 month of age and increased with age. Females showed higher titers than did males. MRL/Mp-+/+ mouse sera also exhibited such activity, though somewhat later in life only in female. Other autoimmune mice, NZB, NZB/NZW F1, and BXSB, demonstrated no such activity in either males or females, young and old. The active component of MRL/l sera was shown to be IgG. F(ab')2 or Fc fragments of MRL/l-IgG lost such activity. Not all IL-3-dependent cell lines, however, responded to MRL/l-IgG. We subcloned MRL-IgG responding and nonresponding clones from FDC-P2 cells and both were still dependent to IL-3. Such nonresponding IL-3-dependent cell lines, however, could be stimulated by the culture supernatant of the responding cell line, FDC-P2/185-4, after being stimulated with MRL/l-IgG. In this culture supernatant, IL-3 was found, thus the existence of an autocrine system was suggested in the IL-3-dependent MRL/l-IgG responding cell line.

Animals↗
PubMed1989

Mechanism of action of GnRH: the participation of calcium mobilization and activation of protein kinase C in gonadotropin secretion.

The role of protein kinase C in luteinizing hormone (LH) release was analyzed in studies on the secretory responses to gonadotropin releasing hormone (GnRH) and phorbol esters in pituitary cell cultures. 12-O-tetradecanoyl-phorbol 13-acetate (TPA), 4 beta-phorbol 12,13-bibenzoate, and 4 beta-phorbol 12,13-diacetate stimulated LH release with ED50s of 5, 10 and 1000 nM, respectively, and with about 70% of the efficacy of GnRH. Phorbol ester-stimulated LH secretion was decreased but not abolished by progressive reduction of [Ca2+] in the incubation medium, and the residual response was identical with that of GnRH in Ca2+-deficient medium. TPA increased [Ca2+]i to a peak after 30 s in normal medium but not in the absence of extracellular Ca2+, indicating that protein kinase C promotes calcium entry but can also mediate secretory responses without changes in calcium influx and [Ca2+]i. The extracellular Ca2+-dependent action of TPA on LH release was blocked by CoCl2 but not by nifedipine. The secretory actions of TPA and GnRH were additive at low doses and converged to a common maximum LH response at high concentrations of the agonists. TPA caused rapid translocation of cytosolic protein kinase C to the particulate fraction, followed by a progressive decrease in total enzyme activity to less than 10% after 6 h. Partial recovery of the cytosolic enzyme (to 20%) occurred after washing and reincubation for 15 h. Such kinase C-depleted cells showed prominent dose-dependent reductions in the actions of both GnRH and TPA on LH release in normal and Ca2+-deficient media. These observations show that the actions of kinase C on LH release include extracellular Ca2+-dependent and independent components, and support the hypothesis that protein kinase C participates in the LH secretory response to GnRH in pituitary gonadotrophs.

Animals↗
PubMed1989

Methods for monitoring follicle maturation decrease; the ovarian hyperstimulation syndrome during gonadotropin treatment.

Therapy with human menopausal gonadotropin and human chorionic gonadotropin (hMG-hCG) has proved effective for induction of ovulation in patients with hypogonadotropic hypogonadism showing anovulation or sterility. However, two important complications, the ovarian hyperstimulation syndrome (OHSS) and multiple gestations, are observed in a few patients treated with these hormones. In the past, follicular maturation was evaluated by the cervical mucus score (CM) and serum estradiol level (E2). But recently, ultrasonographic monitoring (USG) and the measurement of urinary estrogen (E) with a commercial kit of sufficiently high sensitivity have been advocated for the prevention of these complications. In this study, we investigated the relationships between the monitoring methods during hMG-hCG treatment and the rates of the OHSS, ovulation, pregnancy and multiple pregnancy.

Chorionic Gonadotropin↗
PubMed1989

Excitatory effect of histamine on the arousal system and its inhibition by H1 blockers.

To clarify whether the sedative effect of H1 blockers is exerted in relation to H1 receptors in the brain, EEG activity recorded from the cortex and thalamus of rats was studied by power spectral analysis. EEG processing was performed by the FFT method and displayed as compressed spectral arrays. When a train of low frequency electrical stimulation was applied to the midbrain reticular formation of conscious rats, there was an increase in spectral power recorded at the cortex and thalamus, especially in the low frequency bands (0-6 Hz). The intraventricular administration of histamine suppressed the increase in power; this inhibition was antagonized by simultaneous administration of pyrilamine or diphenhydramine, though not in in combination with cimetidine or ranitidine. As in the case of histamine, the administration of 2-methylhistamine decreased power in the slow wave region, while administration of 4-methylhistamine did not. It was assumed that the arousal effect of histamine is exerted via H1 and not related to H2 receptors. Adverse effects of H1 blockers, such as drowsiness, may be caused by their inhibition of histamine's arousal effect.

Animals↗
PubMed1989

Ovulation following combined therapy with wen-jing-tang and clomiphene citrate therapy in anovulatory women.

The effect of combined therapy with Wen-Jing-Tang and clomiphene citrate on anovulation was studied in 16 infertile patients who did not respond to clomiphene citrate alone. Wen-Jing-Tang was given at a dose of 5 g a day every day from day 2 of the menstrual cycles and clomiphene citrate was given at 150 mg a day for 5 days from day 5 of the cycle. Ovulation occurred in 43.8% of the patients and 48.6% of the cycles. No case of ovarian hyperstimulation syndrome or pregnancy were observed. These results suggest that the combined therapy with Wen-Jing-Tang and clomiphene citrate should be used before therapy with human menopausal gonadotropin.

Adult↗
PubMed1989

Mechanism of release of beta-endorphin from rat pituitary cells. Role of lipoxygenase products of arachidonic acid.

We investigated the effects of metabolites of arachidonic acid on the release of beta-endorphin-like immunoreactivity (beta-end-IR) from rat anterior pituitary cells. Anterior pituitary cells from female rats cultured with arachidonic acid released beta-end-IR in a dose- and time-dependent manner. To determine which metabolites of arachidonic acid stimulated the release of beta-end-IR, we examined the effects of an inhibitor of the cyclooxygenase, indomethacin, and an inhibitor of the 5-lipoxygenase, 2,3,5-trimethyl-6-(12-hydroxy-5,10-dodecadiynyl)-1,4-benzoquinone (AA-861). beta-end-IR release from pituitary cells induced by arachidonic acid was inhibited about 37% by AA-861, but was not affected by indomethacin. Other lipoxygenase inhibitors (eicosatetraynoic and nordihydroguaiaretic acid) also reduced the release of beta-end-IR induced by arachidonic acid. The effects of the 5-lipoxygenase products 5-hydroxy-6,8,11,14-eicosatetraenoic acid (5-HETE) and leukotrienes (LTA4, B4, C4, and D4) on the release of beta-end-IR from rat pituitary cells were also examined. 5-HETE (1-50 microM) elicited a dose-dependent release of beta-end-IR from cultured pituitary cells, and 50 microM 5-HETE induced beta-endorphin release time dependently. LTA4 and LTB4 also significantly stimulated the release of beta-end-IR, but LTC4 and LTD4 had no effect. Other lipoxygenase products (12-hydroxy-5,8,10,14-eicosatetraenoic acid, 12-HETE; 15-hydroxy-5,8,10,14-eicosatetraenoic acid, 15-HETE) were also secretagogues at concentrations of above 1 microM.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Influence of aging on the histamine release and membrane fluidity of rat peritoneal mast cells.

The maturational changes in the degree of homologous passive cutaneous anaphylaxis (PCA) and the histamine release from peritoneal mast cells induced by several secretagogues were studied using Wistar rats (4-40 weeks old). Although the increase in vascular permeability of the rat skin induced by intradermal injection of histamine did not change significantly from one maturation period to the next, 6- to 8-weeks old rats were both the most susceptible to PCA reactions and the most responsive to histamine-releasing stimuli. Among rats in this age group (6-8 weeks), the fluidity of the resting cell membrane and the extent of membrane fluidity increase in response to compound 48/80 were greatest. Analysis of the lipid composition of mast cells indicated that the ratio of cholesterol to phospholipids was lowest at the age of 6-8 weeks. From the present study, we concluded that the maturational changes in the extent of histamine release seem to be related to membrane fluidity, which has a profile similar to that of maturation.

Aging↗
PubMed1989

Microfilament-associated, local degranulation of rat peritoneal mast cells.

When compound 48/80 was applied by means of microelectrophoresis to the surface of a rat peritoneal mast cell, localized degranulation was observed in the area close to the microelectrode tip. The extruded granules were connected to the cell surface by filaments. The filaments were elongated radially and, in some occasions, projected to a length of 5 microns. A few minutes later, the length of the protruded filaments became shorter and shorter and, finally, the extruded granules were reincorporated into the cell. When rhodamine-phalloidin, an F-actin-specific dye, was perfused the extruded granules and filaments were stained by this dye. This indicates that actin filaments or fragments of them exist on the granule surface and on the cell surface at the site of degranulation. These actin filaments bound to the mast cell granules may play an important role, not only for the extrusion of the granules, but also for the reuptake of extruded granules into the cytoplasm.

Actin Cytoskeleton↗
PubMed1989

Estrogen stimulates gonadotropin-releasing hormone release from rat hypothalamus independently through catecholamine and histamine in vitro.

Estradiol is known to stimulate gonadotropin-releasing hormone release from the rat medio-basal hypothalamus. Studies were made in an in vitro perifusion system on whether catecholamine and/or histamine was involved in estradiol-induced GnRH release. Normal cycling female rats were decapitated in diestrus II and their medio-basal hypothalami were combined and, perifused with Earl's balanced salt solution containing 0.01% bovine serum albumin bubbled with 95% O2 and 5% CO2. The levels of norepinephrine, dopamine, and histamine and of GnRH in the effluent were measured by HPLC and radioimmunoassay, respectively. Administration of 10(-6) mol/l estradiol resulted in releases of norepinephrine, dopamine, histamine and GnRH at levels of 98, 70, 91 and 288%, respectively, of initial values. Administration of 10(-6) mol/l norepinephrine or dopamine resulted in no increase in histamine release, and administration of 10(-6) mol/l histamine did not increase release of norepinephrine or dopamine. These data suggest that estradiol stimulates the releases of GnRH, catecholamine and histamine from the rat medio-basal hypothalamus, and that it increases GnRH release independently through catecholamine and histamine. As we found previously that norepinephrine or histamine stimulates GnRH release from the medio-basal hypothalamus, we conclude that estradiol stimulates releases of norepinephrine and histamine, resulting in GnRH release from the medio-basal hypothalamus.

Animals↗
PubMed1989

Hydramnios associated with congenital mesoblastic nephroma: case report.

A case is reported of hydramnios due to excessive fetal urine production associated with congenital mesoblastic nephroma. Rapid growth of a right renal tumor and excessive fetal urine production were detected by measuring the size of the tumor and hourly fetal urine production during the development of hydramnios between 28-34 weeks of gestation. A female infant weighing 2200 g was born at 34 weeks' gestation. She lost 18% of her birth weight in the first 48 hours because of neonatal polyuria. Right nephrectomy and ureterectomy were performed 2 days after birth. After the operation, the neonatal polyuria improved dramatically. The right renal tumor was identified histologically as a mesoblastic nephroma. The importance is stressed of early and correct antenatal diagnosis of a renal tumor and precise estimation of urine production for postnatal management of hemodynamic change in cases of mesoblastic nephroma.

Adult↗
PubMed1989

[Antenatal detection of developing nervous system abnormalities and perinatal surgical management].

As the use of prenatal ultrasound sonographic study becomes more popular, it is likely that several fetal anomalies of the central nervous system will be diagnosed in utero more frequently and accurately. Obstetric sonogram correlates well with the results of postnatal CT scanning. Now, with improved diagnosis and support facilities for the newborn, neurosurgical intervention is being requested, as more concern is expressed for such fetus. We have experienced seven cases of fetal disorders of the central nervous system-meningocele, meningoencephalocele, myeloschisis, arachnoid cyst and maximal hydrocephalus. When diagnosed late in gestation (after the 2nd trimester), it may be reasonable to consider early delivery at the time of pulmonary maturity, and extrauterine management to decrease secondary damage to the developing central nervous system. The method of delivering a fetus must be tailored to suit each case. We present our program for the management of fetal hydrocephalus-placement of a subcutaneous low profile Ommaya's reservoir for neonate immediately after birth, and then subsequently conversion to a ventriculoperitoneal shunt three or four weeks later. As advances are made in antenatal diagnostic techniques and appropriate therapy, prognostic data on congenital abnormalities of the central nervous system will increase and become more pertinent.

Arachnoid↗
PubMed1989

Histamine and its actions on isolated tissues of lower vertebrates.

The response to histamine (Hi) of isolated organs such as the intestinal tract and heart, obtained from certain lower vertebrates, was investigated phylogenetically and compared with the response to acetylcholine (ACh), 5-hydroxytryptamine and epinephrine (Ep). Contractions induced by Hi (10(-4) M) were not noticeable in any of the intestinal strips of fish and amphibians tested, although ACh produced marked contractions in all preparations even at 10(-6) M. Contractile responses of intestinal preparations to Hi were elicited from reptiles, and seemed to be associated with the H1 receptor in many species but not with the H2 receptor. In isolated fish auricles, neither inotropic nor chronotropic responses were produced by Hi. In bullfrogs and in the majority of species, including reptiles and higher classes, a marked positive inotropic response was elicited via H1 or H2 receptors, but in some animals chronotropic effect was less impressive. The effects of ACh and Ep on heart preparations were remarkable in almost all species tested. When the Hi contents in various tissues were studied comparatively, a determinant stage of Hi appearance in the tissue coincided with the stage in which a definite Hi response emerged in isolated organs.

Acetylcholine↗
PubMed1988

Histamine incorporation into murine myeloblasts and promyelocytes. Formation of a histamine transport system.

When isolated murine myeloblasts and promyelocytes were treated with 3H-histamine (5 x 10(-7) M) in RPMI-1640 medium supplemented with 20% horse serum at 37 degrees, the radioactivity of these cells increased gradually, reaching a maximum after 6 hr. However, when these progenitor cells were pretreated with unlabeled histamine (5 x 10(-7) M) for 1 hr, subsequent exposure to 3H-histamine caused prompt incorporation, the extent of which was more than 3.8 times that seen in cells which were not pretreated. This acceleration was prevented by simultaneous addition of cycloheximide (4 x 10(-7) M) or actinomycin D (10(-7) M) in the pre-incubation stage. While the microsomal fraction of progenitor cells pretreated with histamine initially yielded a higher binding capacity, that of the plasma membrane fraction rose significantly after 1 hr. Most of the incorporated 3H-histamine was detected as unmetabolized. Non-histone chromatin protein had a higher affinity to 3H-histamine than did the DNA fraction of progenitor cell nuclei. Histamine inhibited myeloperoxidase activity of myeloid progenitor cells selectively and dose-dependently without affecting eosinophil peroxidase. These findings suggest that histamine incorporated into murine myeloblasts and promyelocytes induces the synthesis of a specific protein(s) through interaction with the nucleus, and that these proteins, in turn, may be combined into the cell membrane, where they act as a transport system for histamine incorporation.

Animals↗
PubMed1988

Mechanisms of secretory responses to gonadotropin-releasing hormone and phorbol esters in cultured pituitary cells. Participation of protein kinase C and extracellular calcium mobilization.

The role of protein kinase C in luteinizing hormone (LH) release was analyzed in studies on the actions of gonadotropin releasing hormone (GnRH) and phorbol esters in cultured pituitary cells. During incubation in normal medium, GnRH stimulated LH release with an ED50 of 0.35 nM. Incubation in Ca2+-deficient medium (Ca2+-free, 10 microM) substantially decreased but did not abolish the LH responses to GnRH. The extracellular Ca2+-dependent component of GnRH action could be mimicked by high K+ concentrations, consistent with the presence of voltage-sensitive calcium channels (VSCC) in pituitary gonadotrophs. Ca2+ channel agonist (Bay K 8644) and antagonist (nifedipine) analogs, respectively, enhanced or partially inhibited LH responses to GnRH and also to K+, the latter confirming the participation of two types of VSCC (dihydropyridine-sensitive and -insensitive) in K+-induced secretion. Phorbol esters, including 12-O-tetradecanoylphorbol-13-acetate (TPA), 4 beta-phorbol-12,13-dibenzoate, and 4 beta-phorbol-12,13-diacetate, stimulated LH release with ED50s of 5, 10, and 1000 nM, respectively, and with about 70% of the efficacy of GnRH. Phorbol ester-stimulated LH secretion was decreased but not abolished by progressive reduction of [Ca2+]e in the incubation medium, and the residual LH response was identical with that elicited by GnRH in Ca2+-deficient medium. TPA increased [Ca2+]i to a peak after 20 s in normal medium but not in the absence of extracellular Ca2+, indicating that protein kinase C (Ca2+/phospholipid-dependent enzyme) promotes calcium entry but can also mediate secretory responses without changes in calcium influx and [Ca2+]i. The extracellular Ca2+-dependent action of TPA on LH release was blocked by Co2+. However, nifedipine did not alter TPA action on [Ca2+]i and LH release. These observations indicate that protein kinase C can participate in GnRH-induced LH release that is independent of Ca2+ entry, but also promotes the influx of extracellular Ca2+ through dihydropyridine-insensitive Ca2+-channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗