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Y Kitamura

Publications and source records attributed to Y Kitamura.

At least 469 records · Page 26Linked to original sources
PubMed1993

Inducible nitric oxide synthase in glial cells.

Nitric oxide (NO), a free radical gas, has been suggested to mediate both synaptic plasticity and neuronal death. NO is generated by constitutive and inducible types of NO synthase (cNOS and iNOS, respectively). The neuronal cNOS was recently cloned, sequenced and characterized. In contrast, properties of iNOS in the brain are not fully understood. It is noted that glial cells can form NO and that microglial and reactive astroglial cells are accumulated around neurodegenerative sites in the brain, suggesting a relationship between neuronal injury and NO originated from glial cells. We found that several stimuli such as endotoxin (lipopolysaccharide) and cytokines induced iNOS in glial cells of rat brain. This article reviews recent findings on characteristics and the induction mechanism of iNOS in the glial cells, and discusses the possible pathophysiological functions of iNOS in the brain.

Amino Acid Oxidoreductases↗
PubMed1993

Characterization of [3H]staurosporine binding in protein kinase C-II purified from rat brain.

The type II protein kinase C (PKC-II) densely present in mammalian brain plays functional roles in CNS. We examined the characteristics of [3H]staurosporine binding to PKC-II purified from rat brain, compared to [3H]phorbol 12, 13-dibutyrate (PDBu) binding. In brief, [3H]staurosporine binding increased by phosphatidylserine (PtdSer) in a concentration-dependent manner and the binding was enhanced by Ca2+ and phorbol 12-myristate 13-acetate (PMA). In the presence of Ca2+, PMA and PtdSer, Bmax of these bindings markedly increased, but KD did not change. These characteristics of binding were similar to [3H]PDBu binding to PKC-II. Although [3H]PDBu binding was not affected by protein kinase inhibitors such as staurosporine, H-7, K-252a and K-252b, [3H]staurosporine binding was inhibited by these inhibitors. [3H]staurosporine binding was inhibited by several ATP analogues, but was not by guanine nucleotides. PtdSer-induced increase in [3H]PDBu binding was inhibited by Zn2+, but Zn2+ induced increase in [3H]staurosporine binding as well as PtdSer and/or Ca2+. Staurosporine would thus appear to bind to a domain different from phorbol ester-binding one in PKC, interactions between both domains may regulate kinase activity, and 1 mol staurosporine and 4 mol phorbol ester may bind to 1 mol PKC-II.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1993

Development of mast cells and basophils: processes and regulation mechanisms.

Mast cells and basophils are offspring of the multipotential hematopoietic stem cell. Although mast cells sometimes are misunderstood as basophils that have invaded connective or mucosal tissue, these two kinds of basophilic cells are distinguishable by morphology and surface antigenicity. Developmental processes of mast cells and basophils are different. Basophils complete their differentiation within the bone marrow, but precursors of mast cells leave the bone marrow, invade connective or mucosal tissue, proliferate, and differentiate into mast cells. The mechanisms regulating development are different between mast cells and basophils. Both T cell-dependent and fibroblast-dependent mechanisms are involved in the development of rodent mast cells, but only the fibroblast-dependent mechanism is known for development of human mast cells and only the T cell-dependent mechanism for the development of basophils of both rodents and humans. The most important cytokine for the T cell-dependent mechanism appears to be interleukin-3, whereas for the fibroblast-dependent mechanism it appears to be the ligand for the c-kit receptor (ie, stem cell factor).

Animals↗
PubMed1993

Stimulatory effects of protein kinase C and calmodulin kinase II on N-methyl-D-aspartate receptor/channels in the postsynaptic density of rat brain.

To clarify the regulatory mechanism of the N-methyl-D-aspartate (NMDA) receptor/channel by several protein kinases, we examined the effects of purified type II of protein kinase C (PKC-II), endogenous Ca2+/calmodulin-dependent protein kinase II (CaMK-II), and purified cyclic AMP-dependent protein kinase on NMDA receptor/channel activity in the postsynaptic density (PSD) of rat brain. Purified PKC-II and endogenous CaMK-II catalyzed the phosphorylation of 80-200-kDa proteins in the PSD and L-glutamate- (or NMDA)-induced increase of (+)-5-[3H]methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imi ne maleate ([3H]MK-801; open channel blocker for NMDA receptor/channel) binding activity was significantly enhanced. However, the pretreatment of PKC-II- and CaMK-II-catalyzed phosphorylation did not change the binding activity of L-[3H]glutamate, cis-4-[3H](phosphonomethyl)piperidine-2-carboxylate ([3H]CGS-19755; competitive NMDA receptor antagonist), [3H]glycine, alpha-[3H]-amino-3-hydroxy-5-methyl-isoxazole-4-propionate, or [3H]-kainate in the PSD. Pretreatment with PKC-II- and CaMK-II-catalyzed phosphorylation enhanced L-glutamate-induced increase of [3H]MK-801 binding additionally, although purified cyclic AMP-dependent protein kinase did not change L-glutamate-induced [3H]MK-801 binding. From these results, it is suggested that PKC-II and/or CaMK-II appears to induce the phosphorylation of the channel domain of the NMDA receptor/channel in the PSD and then cause an enhancement of Ca2+ influx through the channel.

Animals↗
PubMed1993

Genetic analysis of double-strand break repair in Escherichia coli.

We had reported that a double-strand gap (ca. 300 bp long) in a duplex DNA is repaired through gene conversion copying a homologous duplex in a recB21 recC22 sbcA23 strain of Escherichia coli, as predicted on the basis of the double-strand break repair models. We have now examined various mutants for this repair capacity. (i) The recE159 mutation abolishes the reaction in the recB21C22 sbcA23 background. This result is consistent with the hypothesis that exonuclease VIII exposes a 3'-ended single strand from a double-strand break. (ii) Two recA alleles, including a complete deletion, fail to block the repair in this recBC sbcA background. (iii) Mutations in two more SOS-inducible genes, recN and recQ, do not decrease the repair. In addition, a lexA (Ind-) mutation, which blocks SOS induction, does not block the reaction. (iv) The recJ, recF, recO, and recR gene functions are nonessential in this background. (v) The RecBCD enzyme does not abolish the gap repair. We then examined genetic backgrounds other than recBC sbcA, in which the RecE pathway is not active. We failed to detect the double-strand gap repair in a rec+, a recA1, or a recB21 C22 strain, nor did we find the gap repair activity in a recD mutant or in a recB21 C22 sbcB15 sbcC201 mutant. We also failed to detect conservative repair of a simple double-strand break, which was made by restriction cleavage of an inserted linker oligonucleotide, in these backgrounds. We conclude that the RecBCD, RecBCD-, and RecF pathways cannot promote conservative double-strand break repair as the RecE and lambda Red pathways can.

Bacterial Proteins↗
PubMed1993

Supernormal histamine release and normal cytotoxic activity of beige (Chédiak-Higashi syndrome) rat mast cells with giant granules.

The beige rat is an animal model of the Chédiak-Higashi syndrome. Since mast cells can be easily purified from the peritoneal cavity of rats, we investigated the function of beige rat mast cells with giant granules by using quantitative methods. Beige and normal rat mast cells were sensitized with anti-dinitrophenol (DNP) IgE antibodies and stimulated by DNP conjugated with human serum albumin. The proportion of histamine released to total histamine was significantly greater in beige rat mast cells than in normal rat mast cells. Since the supernormal histamine release of beige rat mast cells was observed after treatment with 12-O-tetradecanoylphorbol 13-acetate, calcium ionophore A23187, substance P or compound 48/80, it appeared to be attributable to the enlargement in granules in beige rat mast cells. Spontaneous cytotoxic activity of mast cells was assayed by incubating purified mast cells with 51Cr-labelled WEHI-164 cells. Both beige and normal rat mast cells showed significant cytotoxic activity, but no significant difference was detectable between beige and normal rat mast cells. Even after IgE-mediated stimulation, no significant difference in cytotoxic activity was detectable between beige and normal rat mast cells either. Giant granules of beige rat mast cells did not appear to influence the cytotoxic activity of mast cells.

Animals↗
PubMed1993

Neural mechanism of hypertension by nitric oxide synthase inhibitor in dogs.

This study aimed to determine the mechanism of hypertension associated with nitric oxide synthase inhibition. Intravenous injections of NG-nitro-L-arginine, a nitric oxide synthase inhibitor, produced a sustained increase in systemic blood pressure and a decrease in heart rate in anesthetized dogs, whereas NG-nitro-D-arginine had no effect. L-Arginine reversed the pressor response. NG-Nitro-L-arginine-induced hypertension was markedly attenuated or abolished by treatment with hexamethonium; this inhibition was still observed when the blood pressure fall caused by the ganglionic blocking agent was compensated by continuous infusion of angiotensin II. In dogs treated with phentolamine in a dose sufficient to lower blood pressure to the level similar to that elicited by hexamethonium and to suppress the pressor response to norepinephrine, the hypertensive effect of NG-nitro-L-arginine was not attenuated. We conclude that hypertension caused by the nitric oxide synthase inhibitor is associated with an elimination of nitroxidergic neural function rather than an impairment of the basal release of nitric oxide from the endothelium.

Amino Acid Oxidoreductases↗
PubMed1993

Expression and localization of oxytocin receptor gene in human uterine endometrium in relation to the menstrual cycle.

The expression of oxytocin receptor mRNA in the human uterus was investigated by polymerase chain reaction after mRNA reverse transcription; in addition, the mRNA was localized by means of in situ hybridization histochemistry. Strong positive signals were observed in myometrial cells at parturition. In nonpregnant human uterine endometrium, oxytocin receptor mRNA was expressed in glandular epithelial cells, but was not observed in stromal cells. The signal in the epithelial cells was stronger at the time of ovulation than during any other phase. The sequential changes in oxytocin receptor mRNA expression in nonpregnant endometrium suggest some alternative biological function of oxytocin in endometrium during the menstrual cycle.

Base Sequence↗
PubMed1993

Stem cell factor induces outgrowth of c-kit-positive neurites and supports the survival of c-kit-positive neurons in dorsal root ganglia of mouse embryos.

The c-kit receptor tyrosine kinase is highly expressed by about 10% of the neurons in the dorsal root ganglia (DRGs) of mouse embryos. We investigated the in vitro effect of stem cell factor (SCF), the ligand for c-kit receptor, on DRGs. Recombinant murine SCF (rmSCF) induced the outgrowth of c-kit-positive neurites from DRGs of normal (+/+) embryos. The effect of SCF was dose dependent and completely abolished by anti-c-kit ACK2 monoclonal antibody (mAb). Some neurites whose outgrowth was induced by nerve growth factor (NGF) were c-kit-positive, but anti-NGF mAb did not inhibit the rmSCF-induced neurite outgrowth. rmSCF did not induce neurite outgrowth from DRGs of W/W embryos that did not express c-kit receptors on the cell surface and of W42/W42 mutant embryos that expressed c-kit receptors without tyrosine kinase activity. rmSCF also had a trophic effect on c-kit-positive neurons in the culture of dissociated DRG cells. Most c-kit-positive neurons appeared to respond to NGF as well, and the SCF-responsive subpopulation represented about 10% of NGF-responsive neurons. rmSCF did not support the survival of DRG neurons from embryos of W/W and W42/W42 genotypes. These results suggest that the stimulus through the c-kit receptor tyrosine kinase has an important role in development of the peripheral nervous system.

Animals↗
PubMed1993

Restriction fragment length polymorphisms (RFLPs) of medicinal plants and crude drugs. I. RFLP probes allow clear identification of Duboisia interspecific hybrid genotypes in both fresh and dried tissues.

A simple and efficient method for identification of Duboisia leichhardtii F. Muell, D. myoporoides R. BR. and their interspecific hybrid was established by analyzing restriction fragment length polymorphism (RFLP) profiles using non-radioactive rice ribosomal DNA as a probe. This procedure was shown to be applicable to both fresh and dried samples, and also suitable for detection of somatic hybrid at the callus stage after protoplast fusion.

DNA↗
PubMed1993

Effects of hormones, cyclic AMP analogues and growth factors on steel factor (SF) production in mouse Sertoli cell cultures.

Regulation of steel factor (SF) production in Sertoli cells from postnatal mouse testes was studied in a mast cell-Sertoli cell coculture system. Treatment of Sertoli cells with dibutyryl cAMP (50-1000 mumol l-1), forskolin (1-25 mmol l-1), and cholera toxin (10 micrograms ml-1) increased SF production, whereas FSH and theophylline had no significant effect. Furthermore, growth factors and testosterone, which would play some roles in spermatogenesis, were also tested, but none of these stimulated SF production. The constitutive production of SF may, rather, reflect the physiological condition of Sertoli cells in vivo.

Animals↗
PubMed1993

[A case of prostatic carcinoma with ectopic ACTH syndrome].

A 67-year-old man was admitted to the orthopedic ward, complaining of severe pain in his right greater trochanter. He was diagnosed as spinal cord tumor and underwent laminectomy for extirpation of the tumor. Histological examination revealed bone metastasis of unknown origin. Laboratory data revealed hypokalemia and hyperglycemia. Endocrinological data showed elevation of plasma cortisol and ACTH, and increased excretion of urinary 17-OHCS. Ten specimens needle biopsy of the prostate showed poorly differentiated adenocarcinoma, thus patient was diagnosed as prostate cancer with bone metastasis (stage D2) and perhaps ectopic ACTH production. Castration was performed, however 2 days after the surgery he died suddenly. We suspected that cerebral hemorrhage was the cause of his death. On autopsy ectopic ACTH production in the prostate was confirmed.

ACTH Syndrome, Ectopic↗
PubMed1993

[Comparative study on urinary parameters reflecting renal damage during chemotherapy for urological cancer].

We analyzed the excretion of the three urinary enzymes, N-acetyl-beta-D-glucosaminidase (NAG), alanine aminopeptidase (AAP), and glycyl-prolyl dipeptidyl aminopeptidase (GP-DAP) and the three urinary proteins, beta-microglobulin (beta 2-M), alpha-microglobulin (alpha 1-M), and albumin during the intravenous administration of anti cancer drugs in 4 prostatic cancer patients and 16 urothelial cancer patients. The patients with prostatic cancer were treated with VIP (vincristine, ifosfamide, peplomycin) chemotherapy and the patients with urothelial cancer were treated with MP (methotrexate, cisplatinum) or MEP (methotrexate, Etoposide, cisplatinum) combination chemotherapy. beta 2-M was the best parameter for drug-induced renal damage because of its sharp and large reactivities. Any urinary enzyme or protein especially albumin which had showed a markedly high value before the chemotherapy was not suitable as a urinary drug-induced renal damage parameter. There was a close resemblance in reactivity pattern between GP-DAP and AAP probably because of the same localization of these enzymes in the renal tubular bruch borders. In the patients with renal damage by chemotherapy, all parameters were changed showing two peaks or persisted with high values.

Acetylglucosaminidase↗
PubMed1993

Absence of immature mast cells in the skin of Ws/Ws rats with a small deletion at tyrosine kinase domain of the c-kit gene.

Ws/Ws rats have a small deletion at the tyrosine kinase domain of the c-kit gene, and practically no mast cells were detectable when the tissues were stained with alcian blue. Because alcian blue stains proteoglycans, there is a possibility that immature mast cells that do not contain a sufficient amount of proteoglycans are not detectable by this method. We examined this possibility by using other markers of mast cells. The histamine content in the skin of Ws/Ws rats was 0.3% that of control normal (+/+) rats. Because the number of alcian blue-positive mast cells in the skin of Ws/Ws rats was also 0.3% that of +/+ rats, histamine in the skin seemed to be concentrated to alcian blue-positive mast cells. Mast cells in the skin of +/+ rats express messenger RNA of Fc epsilon RI beta-subunit and c-kit protein. Because c-kit messenger RNA was normally expressed at least in the brain of Ws/Ws rats despite the small deletion, we examined the expression of Fc epsilon RI beta-subunit and c-kit messenger RNA in the skin and stomach of Ws/Ws rats by reverse transcriptase modification of polymerase chain reaction. Expression of either Fc epsilon RI beta-subunit or c-kit messenger RNA in the skin and stomach of Ws/Ws rats was estimated to be less than 1% that of +/+ rats. Moreover no Fc epsilon RI beta-subunit-expressing and no c-kit-expressing cells were detectable in the skin of Ws/Ws rats by in situ hybridization histochemistry. The present result suggests the absence of immature mast cells in tissues of Ws/Ws rats.

Animals↗
PubMed1993

Nitric oxide-mediated retinal arteriolar and arterial dilatation induced by substance P.

PURPOSE: The present study was undertaken to compare vasodilatations caused by substance P in retinal arterioles in vivo and in the extraocular retinal central arteries in vitro, and to analyze the mechanisms of its action. METHODS: In the in vivo study, changes of the retinal arteriolar diameter were continuously measured using a retinal fundus camera. In the in vitro study, changes in the isometric tension were recorded in helical strips of extraocular retinal arteries with and without the endothelium, exposed to aerated bathing media. RESULTS: In anesthetized dogs, infusions of substance P into the carotid artery produced a dose-dependent dilatation of the intraocular retinal arteriole; the maximal response was obtained about 15 seconds later. The vasodilator response was significantly attenuated by treatment with NG-nitro-L-arginine (L-NA), a nitric oxide (NO) synthase inhibitor, and the inhibition was reversed by L-arginine. On the other hand, vasodilatations caused by nitroglycerin were not influenced by L-NA and L-arginine. In the isolated retinal artery just before entering into the eyeball, the addition of substance P produced a concentration-dependent relaxation only when the endothelium of the strips was intact. Removal of the endothelium abolished the response. The peptide-induced relaxation was abolished by L-NA, whereas relaxations caused by NO and nitroglycerin were unaffected. The inhibitory effect of L-NA was reversed by L-arginine but not by D-arginine. Treatment with methylene blue or oxyhemoglobin abolished the relaxation induced by substance P, NO, and nitroglycerin. CONCLUSIONS: Substance P-induced retinal arteriolar dilatation in vivo appears to be mediated by NO synthesized from L-arginine possibly in the endothelium. The endothelium-dependency would be supported by the findings obtained from isolated retinal arteries.

Animals↗
PubMed1993

Possible involvement of c-kit receptor and its ligand in increase of mast cells in neurofibroma tissues.

Many mast cells are present in the tumor tissues of neurofibromatosis 1. We investigated the mechanism of the mast cell increase. Since the stem cell factor (SCF) induces development of mast cells and since the receptor of SCF is encoded by the c-kit gene, we examined the expression of SCF mRNA and c-kit mRNA in neurofibroma tissues. In situ hybridization demonstrated strong expression of c-kit messenger RNA in mast cells in the neurofibroma, but the expression of SCF mRNA was not demonstrable by in situ hybridization in either neurofibroma tissues or control normal skin tissues. When RNA extracted from neurofibroma tissues or normal skin tissues was reverse transcribed and then amplified by the polymerase chain reaction, the amount of SCF cDNA was greater in neurofibroma tissues than in normal skin tissues. The results suggest that SCF and the c-kit receptor are associated with the increase of mast cells in neurofibroma tissues.

Adolescent↗