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Biomedical subjects

S Kitayama

Publications and source records attributed to S Kitayama.

At least 91 records · Page 5Linked to original sources
PubMed1990

[Contingent negative variation prior to phonation in cleft palate-operated patients].

In an attempt to objectively measure psychological tension suffered by cleft palate-operated patients (CPs) with speech difficulty, the contingent negative variation (CNV) was recorded in CPs and normal subjects. The CNV is an expectancy-related brain potential recorded from the surface of the head. It begins to develop after the warning signal and reaches its maximum before the imperative signal, immediately after which a specific voluntary movement is promptly executed. The maximum amplitude of CNVs and the area encircled by each CNV and its base line were measured in the vertex and the left front-parietal region (FP) during tasks of sound production (voice CNV) or finger flexion (finger CNV). Significant differences between CPs and normals were found in the following CNV parameters: 1) The FP/vertex ratio of the amplitude of finger CNVs was smaller in CPs. 2) The amplitude of voice CNVs in the FP was lower in CPs when normals uttered a Japanese vowel "a" at a relatively low intensity (60 dB) while CPs uttered "a" or the sounds most difficult for them. 3) The ratio of the amplitude of voice CNVs led from the FP to that led simultaneously from the vertex was smaller in CPs during the tasks described in 2. 4) The ratio of the area of voice CNVs in the FP to the amplitude of each CNV was greater in CPs in two cases; firstly in the task where normals uttered "a" and CPs produced the sounds most difficult for them, and secondly in the task where the subjects were asked to make the articulation at a high sound level (80 dB).(ABSTRACT TRUNCATED AT 250 WORDS)

Cleft Palate↗
PubMed1989

Localization of gonadotropin binding sites in human ovarian neoplasms.

The binding of human luteinizing hormone and human follicle-stimulating hormone to ovarian tumor biopsy specimens from 29 patients was analyzed. The binding sites for human luteinizing hormone were demonstrated in one tumor of epithelial origin (mucinous cystadenoma) and in one of sex cord-stromal origin (theca cell tumor). The binding sites for human follicle-stimulating hormone were found in three tumors of epithelial origin (serous cystadenoma and mucinous cystadenoma) and in two of sex cord-stromal origin (theca cell tumor and theca-granulosa cell tumor). The surface-binding autoradiographic study revealed that the binding sites for gonadotropins were localized in the stromal tissue. The results suggest that gonadotropic hormones may play a role in the growth and differentiation of a certain type of human ovarian neoplasms.

Adolescent↗
PubMed1989

A new method of intra-oral open reduction using a screw applied through the mandibular crest of condylar fractures.

As a result of dry skull morphometry on 50 mandibles, the author has obtained evidence that the mandibular crest, the protuberance between the retromolar trigone and the condylar process, was the thickest portion of the ascending ramus of the mandible. This anatomical structure is available for osteosynthesis of condylar fractures when an appropriate surgical procedure is developed and applied. In this paper, a new intra-oral approach technique is presented which is devised for osteosynthesis of condylar fractures using a cancellous bone screw primarily applied through the mandibular crest.

Adult↗
PubMed1989

[A case of recurrent endometrial cancer (clear cell adenocarcinoma) remarkably responsive to combination chemotherapy containing cisplatin].

A 60-year-old woman with recurrent stage II endometrial cancer (clear cell adenocarcinoma) was treated with combination chemotherapy containing cisplatin (CDDP). She had undergone abdominal radical hysterectomy (Okabayashi operation) and pelvic lymph node dissections. Endometrial cancerous tissue infiltrated the cervix and lymph nodes. Six months after the operation, the patient had ascites and dyspnea. She was given 25 mg CDDP intra-abdominally and combination chemotherapy containing CDDP (CAP: CDDP 100 mg, ADR 30 mg, CAP 500 mg) three times intravenously. After an administration of CDDP and combination chemotherapy, the amount of ascites and the serum level of CA 125 decreased remarkably. Although the combination chemotherapy containing CDDP for gynecological malignancy has not been sufficiently evaluated as for ovarian carcinomas, the therapy deserves further evaluation in patients with recurrent of endometrial cancer.

Adenocarcinoma↗
PubMed1988

Evidence that prostaglandins activate calcium channels to enhance basal and stimulation-evoked catecholamine release from bovine adrenal chromaffin cells in culture.

The effects of prostaglandins (PGs) on catecholamine (CA) secretion and Ca2+ fluxes were studied in a primary culture of bovine chromaffin cells. PGD2, PGF2 alpha and PGE2 induced CA release from cultured bovine chromaffin cells in a concentration dependent manner (0.03-3 microM). PGD2, PGF2 alpha and PGE2 at 3 microM elicited maximum CA release of 0.043 +/- 0.001, 0.059 +/- 0.008, 0.062 +/- 0.002 micrograms/10(6) cells, respectively. Three micromolar of PGD2, PGF2 alpha and PGE2 enhanced CA release induced by acetylcholine (ACh) in a degree of 186 +/- 10, 206 +/- 6, 150 +/- 4% of control respectively. PGs also enhanced CA release induced by 20 mM K+, veratridine and A23187. In Ca2+-free medium, PGs failed to affect basal and caffeine (50 mM)-induced CA release. PGF2 alpha increased 45Ca uptake and showed additive effect with ACh on 45Ca uptake. Nicardipine (0.1-10 microM) suppressed CA release and 45Ca uptake induced by PGF2 alpha, while diltiazem and verapamil failed to affect these responses to PGF2 alpha. BAY K 8644 (1 microM) potentiated CA release and 45Ca uptake evoked by PGF2 alpha. These results suggest that PGs enhance basal and stimulation-evoked CA release from chromaffin cells possibly through facilitation of Ca2+ influx. The mechanisms of action of PGs in adrenal medulla are discussed.

Acetylcholine↗
PubMed1988

Potassium-ion activity in the trigeminal central nervous complex during tooth pulp-evoked slow mass potentials.

Following electrical stimulation of the tooth pulp, extracellular K+ activity was enhanced by up to 0.1 mM only in the trigeminal motor nucleus which gave a positive slow mass potential (SMP) of low amplitude. No nuclear region giving a positive or negative SMP of high amplitude showed any detectable change. There are possible generation mechanisms of the negative and positive SMP.

Animals↗
PubMed1988

Isolation of a DNA-binding protein from Deinococcus radiodurans having an affinity for a Z-form polynucleotide.

A protein which preferentially binds Z-form duplex DNA has been purified from the cells of Deinococcus radiodurans. The molecular weight of the protein was estimated to be approximately 68,000 by gel filtration and SDS-polyacrylamide gel electrophoresis. Amino acid analysis of the protein indicates that it is not so basic since it contains a lower mole percent of lysine and higher mole percent of aspartic acid than those in histone-like DNA binding protein II (HU) of Escherichia coli. The first fifteen amino acid residues from the N-terminus have been also determined.

Amino Acids↗
PubMed1987

Modulation during sleep of the cat trigeminal neurons responding to tooth pulp stimulation.

Sleep-induced changes in the trigeminal neuron responses to electrical stimulation of the cat tooth pulp were studied. Two parameters were adopted: One was the evoked spike number at two times the threshold intensity (2 X T response magnitude), which would reveal the level shifting of the neuronal response by the sleep-regulatory system. Another was the rate of change in the response intensity when the stimulus was raised to a level of 0.7 time the arousal threshold during light slow wave sleep (sensitivity gradient), which would reflect the influences of the pain-modulatory system driven by strong noxious inputs. It was found that during sleep the two indexes tended to show a correlated change; the neurons which came to have a greater 2 X T response magnitude tended to have a smaller sensitivity gradient than during wakefulness, and vice versa. It was suggested that two contrasting populations of tooth pulp neurons might be differentiated, and that the sleep-regulatory system and the pain-modulatory system would have differential but correlated controls over these two kinds of neurons.

Animals↗
PubMed1987

Enhancement of stimulation-evoked catecholamine release from cultured bovine adrenal chromaffin cells by forskolin.

Acetylcholine (ACh) increased cyclic AMP levels in cultured bovine chromaffin cells with a peak effect at 1 min after the addition. Pretreatment with forskolin (0.3 microM) enhanced the ACh-evoked cyclic AMP increase. The catecholamine (CA) release induced by ACh was enhanced by forskolin, but forskolin alone did not enhance the CA release. The effect of forskolin increased dose-dependently up to 1 microM, but decreased at higher concentrations. Dibutyryl cyclic AMP (DBcAMP) also enhanced ACh-evoked CA release, but the effect was less potent than that of forskolin. Forskolin enhanced both [3H]norepinephrine ([3H]NE) and endogenous CA release evoked by 30 mM K+ from cells that were preloaded with [3H]NE. The effects of forskolin were substantial when CA release was evoked with low concentrations of ACh or excess K+, but decreased with higher concentrations of the stimulants. Forskolin also enhanced the CA release induced by ionomycin and veratrine, or by caffeine in Ca2+-free medium. The potentiation by forskolin of the ACh-evoked CA release was manifest in low Ca2+ concentrations in the medium, but decreased when Ca2+ concentration was increased. These results suggest that cyclic AMP may play a role in the modulation of CA release from chromaffin cells.

Acetylcholine↗
PubMed1987

Stimulation-evoked Ca2+ fluxes in cultured bovine adrenal chromaffin cells are enhanced by forskolin.

Forskolin, 1 microM, increased acetylcholine (ACh)-stimulated 45Ca uptake by chromaffin cells. The stimulatory effects of forskolin decreased with increasing concentration of ACh. The attenuation of the effect of forskolin on 45Ca uptake as a function of ACh concentration correlated well with changes in the forskolin effect on ACh-evoked catecholamine (CA) release. Forskolin increased excess KCl- and veratrine-evoked CA release and 45Ca uptake. Forskolin by itself stimulated 45Ca efflux and enhanced ACh-, excess KCl-, and veratrine-stimulated 45Ca efflux. High doses of forskolin inhibited both ACh-evoked 45Ca uptake and CA release. The inhibitory action of forskolin was specific to receptor-mediated response because excess KCl- and veratrine-stimulated 45Ca uptake and CA release were not inhibited. Forskolin, 0.3-30 microM, dose-dependently increased caffeine-stimulated CA release and 45Ca efflux in the absence of Ca2+ in the medium, and the effects were mimicked by dibutyryl cyclic AMP. These results suggest that cyclic AMP increases stimulation-induced CA release by enhancing calcium uptake across the plasma membrane and/or altering calcium flux in an intracellular calcium store.

Acetylcholine↗
PubMed1987

Gonadotropin binding sites in human ovarian follicles and corpora lutea during the menstrual cycle.

Gonadotropin binding sites were localized by autoradiography after incubation of human ovarian sections with 125I-labeled gonadotropins. The binding sites for 125I-labeled human follicle-stimulating hormone (125I-hFSH) were identified in the granulosa cells and in the newly formed corpora lutea. The 125I-labeled human luteinizing hormone (125I-hLH) binding to the thecal cells increased during follicular maturation, and a dramatic increase was preferentially observed in the granulosa cells of the large preovulatory follicle. In the corpora lutea, the binding of 125I-hLH increased from the early luteal phase and decreased toward the late luteal phase. The changes in 3 beta-hydroxysteroid dehydrogenase activity in the corpora lutea corresponded to the 125I-hLH binding. Thus, the changes in gonadotropin binding sites in the follicles and corpora lutea during the menstrual cycle may help in some important way to regulate human ovarian function.

3-Hydroxysteroid Dehydrogenases↗
PubMed1986

Increase in catecholamine release and 45Ca2+ uptake induced by GABA in cultured bovine adrenal chromaffin cells.

The role of Ca2+ in GABA-evoked catecholamine (CA) release from adrenal medulla was investigated in primary cultures of bovine adrenal chromaffin cells. GABA facilitated the 45Ca2+ uptake associated with the increase of Ca release in cultured bovine adrenal chromaffin cells. The effects of GABA on both 45Ca2+ uptake and CA release were blocked by bicuculline and picrotoxin. Nifedipine reduced the 45Ca2+ uptake and CA release induced by GABA. These data support our previous suggestion that the activation of GABA receptors on adrenal chromaffin cells facilitates the Ca2+ influx through voltage-sensitive Ca2+ channels, leading to the release of CA.

Adrenal Glands↗
PubMed1986

Potassium ion is indispensable to the catecholamine releasing response of dog adrenals to gamma-aminobutyric acid.

The effect of potassium ion on the GABA-evoked catecholamine (CA) release from isolated perfused adrenal glands of the dog was investigated. When omitting the external potassium ion, the basal release of CA was increased. During this period GABA no longer caused the increase in CA release and moreover the increased basal release was diminished reversibly by GABA. 3-Amino-1-propane-sulfonic acid, a GABAA agonist, mimicked the action of GABA in K+-free solution, while baclofen, a GABAB agonist, did not cause CA release in normal solution and did not alter the basal release in K+-free solution. The inhibition by GABA of the basal CA release in K+-free solution was blocked by bicuculline. The potency of the CA releasing action of GABA was dependent on the concentration of external K+ between 1-10 mM. Reintroduction of K+ to glands which had been perfused with K+-free solution immediately reduced the basal release of CA whereas it recovered the CA releasing action of GABA. These results suggest that GABA-evoked CA release is dependent on potassium ion. The possible mechanisms by which GABA evoked CA release are discussed.

Adrenal Glands↗
PubMed1986

Forskolin enhancement of acetylcholine-evoked cyclic AMP formation and catecholamine release in perfused dog adrenals.

Unstimulated efflux of cyclic AMP from perfused dog adrenal glands was not altered by 0.1 microM of forskolin and was slightly increased by 0.3 and 1.0 microM of forskolin. ACh stimulated efflux of cyclic AMP which preceded CA release and the efflux was dose-dependently enhanced by forskolin. Forskolin did not affect the spontaneous CA release but enhanced ACh-evoked catecholamine (CA) release. There was a close correlation between the dose relationship of forskolin enhancement of stimulated-cyclic AMP efflux and that of evoked-CA release. ACh-evoked CA release in the presence of forskolin was further potentiated by R020-1724, a phosphodiesterase inhibitor. CA release evoked by excess K+, or by caffeine in the presence or absence of external Ca2+ was also potentiated by forskolin. These results suggests that cyclic AMP generation may increase in response to stimulation of adrenal chromaffin cells and that the resulting increase of the nucleotide may function as a facilitating modulator of CA release.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗
PubMed1986

Mechanism of radiosensitizing effect of chloride ion on E. coli.

Cells of E. coli capable of repairing DNA damage are sensitized to radiation in the presence of NaCl. However, the enhanced radiolethality was suppressed by the addition of compounds such as an amino acid to the irradiation buffer. The protective efficiencies of these compounds depend on their reactivities with Cl-.2 or OH.. ATP synthesis in the cells irradiated in the presence of NaCl was severely inhibited depending on the dose of irradiation. This reduced rate of ATP synthesis can account for the inhibition of protein, RNA and DNA synthesis in the irradiated cells with NaCl.

Adenosine Triphosphate↗
PubMed1986

Facilitation of acetylcholine-evoked catecholamine release by cyclic AMP on isolated perfused dog adrenal glands.

The effects of cyclic nucleotides on catecholamine (CA) release and Ca2+ efflux were determined on isolated dog adrenals perfused with 1.3 mM Ca2+ containing fluid except indicated. Dibutyryl cyclic AMP (DBcAMP, 50 microM--1 mM) substantially enhanced CA release evoked by acetylcholine (ACh) and slightly increased the spontaneous CA release. Dibutyryl cyclic GMP (100-500 microM) narrowly increased the basal CA release. DBcAMP, 200 microM also significantly facilitated CA release caused by nicotine, bethanechol and excess K+, and by caffeine in the absence of extracellular Ca2+. 45Ca efflux evoked by ACh and by caffeine in the absence of extracellular Ca2+ from prelabelled adrenals with 45Ca was enhanced significantly by DBcAMP, 200 microM. These results suggest that cAMP may function as a facilitatory modulator in CA release from the adrenal medulla via in part the effect on Ca2+ flux including alterations in the function of systems for intracellular Ca2+ homeostasis.

Acetylcholine↗