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Y Hattori

Publications and source records attributed to Y Hattori.

At least 19 recordsLinked to original sources
PubMed1992

K-sam-related gene, N-sam, encodes fibroblast growth factor receptor and is expressed in T-lymphocytic tumors.

We recently reported the isolation of the K-sam complementary DNA (cDNA), which was amplified preferentially in poorly differentiated types of stomach cancer and codes for one of the heparin-binding growth factor or fibroblast growth factor (FGF) receptor families. The K-sam-related gene, N-sam (NCC-IT-cell-derived sam), was isolated by screening of the cDNA libraries of human immature teratoma cells, NCC-IT. Sequence analysis of the N-sam cDNAs showed that N-sam encodes a human FGF receptor, the FLG protein. N-sam was expressed in lymphocytic leukemia/lymphoma cells, predominantly in the thymic T-cell phenotype. In a T-cell leukemia line, MOLT3, N-sam mRNA expression was markedly enhanced by 12-O-tetradecanoylphorbol-13-acetate treatment and was also up-regulated by basic FGF exposure. These results indicate that N-sam expression is regulated during T-cell ontogeny and modulated by its putative ligand exposure. The results also suggested that interaction between immature T-cell and marrow or thymic interstitial cells might be mediated by N-sam and basic FGF stored in the extracellular matrix of stromal cells.

Base Sequence↗
PubMed1992

K-sam gene encodes secreted as well as transmembrane receptor tyrosine kinase.

K-sam was first identified as a gene amplified in the stomach cancer cell line KATO-III. The size of the major transcript of the K-sam gene was 3.5 kilobases in KATO-III cells, and we have previously shown that K-sam encodes a receptor tyrosine kinase that belongs to the heparin-binding growth factor receptor, or fibroblast growth factor receptor, gene family. The K-sam gene expresses multiple sizes of mRNAs in brain tissue, the immature teratoma cell line NCC-IT, and KATO-III. RNA blot analyses with a variety of K-sam probes indicate that there are at least four classes of K-sam mRNAs. Three types of K-sam cDNAs in addition to the previously reported type of K-sam cDNA were isolated, and their nucleotide sequences encode a full-length transmembrane receptor, a secreted receptor with a tyrosine kinase domain, and a secreted receptor without a tyrosine kinase domain.

Base Sequence↗
PubMed1992

Glibenclamide does not block arterial relaxation caused by vasoactive intestinal polypeptide.

Vasoactive intestinal polypeptide (VIP) caused a concentration-dependent relaxation in rabbit mesenteric artery with intact endothelium. The relaxant response to VIP was inhibited by the removal of the endothelium or by pretreatment with methylene blue, but not by pretreatment with glibenclamide. A small but significant relaxant response to VIP in the endothelium-denuded artery was also unaffected by glibenclamide. These findings indicate that ATP-sensitive K+ channels are not involved in the endothelium-dependent or endothelium-independent arterial relaxation elicited by VIP.

Animals↗
PubMed1992

Expression of the heparin-binding growth factor receptor genes in human megakaryocytic leukemia cells.

K-sam/bek, N-sam/flg and FGFR3/sam3 establish gene family of the receptors for heparin-binding growth factors (HBGFs) or FGFs. These mRNAs were detected in human leukemia cells, CMK, K562 and HEL, which have megakaryocytic phenotype or the potency to differentiate into megakaryocytic lineage. In CMK cells N-sam/flg transcript level was enhanced by the culture with 12-O-tetradecanoylphorbol-13-acetate (TPA). cDNA-polymerase chain reaction identified K-sam/bek mRNA in human platelets, suggesting the involvement of HBGFs in megakaryocytopoiesis and functions of platelets.

Base Sequence↗
PubMed1992

Electrophysiologic and anticholinergic effects of pirmenol enantiomers in guinea-pig myocardium.

Since it has been reported that several class I drugs stereoselectively block sodium channels, potassium channels and muscarinic receptors in cardiac tissues, electrophysiologic and anticholinergic effects of enantiomers of pirmenol, a class I antiarrhythmic drug, were examined. Both (+) and (-) pirmenol depressed the maximum upstroke velocity (Vmax) of the action potential in a concentration-dependent manner in guinea-pig papillary muscles driven at 1.0 Hz, and there was no significant difference in the potency of the class I effect between the enantiomers. The onset rates of use-dependent block (UDB) of Vmax at 2.0 Hz for 10 mumol/l (+) and (-) pirmenol were 0.30 +/- 0.03 and 0.29 +/- 0.01 per action potential, and the recovery time constants from UDB for (+) and (-) pirmenol were 27.0 +/- 2.7 and 27.7 +/- 1.9 s, respectively, indicating no difference in the binding and unbinding kinetics to the sodium channel between the enantiomers. Both (+) pirmenol and (-) pirmenol prolonged action potential duration (APD) at low concentrations (1-10 mumol/l) and shortened it at high concentrations (30-100 mumol/l). Again, there was little difference with respect to the effects on APD between the enantiomers. However, in the isolated guinea-pig left atria (-) pirmenol more potently antagonized the negative inotropic effect of carbachol than (+) pirmenol, and the pA2 values for (+) and (-) pirmenol were 6.41 and 6.71, respectively. The functional study was supported by the radioligand binding experiments using [3H]N-methylscopolamine ([3H]NMS) in guinea-pig left atrial membranes.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1992

Development of epileptic activity induced by iron injection into rat cerebral cortex: electrographic and behavioral characteristics.

Unilateral injection of ferrous chloride solution into the rat sensorimotor cortex produced epileptic discharges in the electrocorticograms (ECoGs). The discharges were isolated spikes and spike and wave complexes, and the epileptic activity lasted for more than 12 months after the injection. Isolated spike activity often appeared on the left or right side of the cortex, whereas spike and wave complex activity appeared bilaterally. In rats showing dominant isolated spike activity in the secondary epileptic cortex, there was a deviation in somatosensory evoked potentials (SEPs). Rats showing isolated spikes and spike and wave complexes exhibited vibrissa tremors and head nodding. Rats showing only isolated spikes exhibited no abnormal behavior, but their convulsion thresholds to pentylenetetrazol were lowered. The results including ECoGs, SEPs, behavior and convulsion threshold were characterized with reference to the development of iron-induced epilepsy. The profiles of ECoG discharge activity and SEP configuration suggest that the process of iron-induced epilepsy consists of 3 stages.

Animals↗
PubMed1992

Effects of inorganic iodide, epidermal growth factor and phorbol ester on hormone synthesis by porcine thyroid follicles cultured in suspension.

Porcine thyroid follicles cultured in suspension for 96 h synthesized and secreted thyroid hormones in the presence of thyrotropin (TSH). The secretion of newly synthesized hormones was assessed by determining the contents of thyroxine (T4) and triiodothyronine (T3) in the media and by paperchromatographic analysis of 125I-labelled hormones in the media where the follicles were cultured in the presence and absence of inhibitors of hormone synthesis. The hormone synthesis and secretion was modified by exogenously added NaI (0.1-100 microM). The maximal response was obtained at 1 microM. Thyroid peroxidase (TPO) activity in the cultured follicles with TSH for 96 h was dose-dependently inhibited by NaI. One hundred microM of NaI completely inhibited TSH-induced TPO activity. Moreover, both epidermal growth factor (EGF: 10(-9) and 10(-8) M) and phorbol 12-myristate 13-acetate (PMA: 10(-8) and 10(-7) M) inhibited de novo hormone synthesis. An induction of TPO activity by TSH was also inhibited by either agent. These data provide direct evidences that thyroid hormone synthesis is regulated by NaI as well as TSH at least in part via regulation of TPO activity and also that both EGF and PMA are inhibitory on thyroid hormone formation.

Animals↗
PubMed1992

Further characterization of cortical polarization-induced motor behavior in rabbits.

Anodal direct currents of 1 or 10 microA were unilaterally applied for 30 min once a day to the premotor area of the cerebral cortex in rabbits, in which the current application was repeated 10 times at intervals of 2-3 days. Peripheral motor behavior was observed during and after each polarization trial, and was compared with that before polarization. The motor manifestations were classified into two types: gentle flexion of either forelimb and struggle with violent movement of forelimbs. Flexion of the forelimb contralateral to the polarized cortical side was clearly increased by polarization at an intensity of 1 microA, but not at 10 microA. Forelimb struggle of both sides decreased only when 10 microA was applied. These results suggest that the passage of 1 microA current activates the polarized local area of the cortex, while 10 microA has an inhibitory effect on cortical activity.

Animals↗
PubMed1992

Electron microscopic study of vascular regeneration in rat tracheal mucosa following physical curettage.

Transmission and scanning electron microscopic studies were made of regeneration of the vascular network of rat tracheal mucosa on 30 min to 8 hr after the mechanical curettage. The vascular network casts were made by infusion of Mercox resin through the aortic arch for scanning electron microscopy. At 30 min after curettage, vascular thromboses were observed, and terminal blind branches were formed in the injured blood vessels areas through SEM observation. Diapedesis of leukocytes appeared at 30 min after curettage from intact venules at the wound margins. Recovery from the loss of endothelial cells began at 30 min after curettage. At 3 hr after curettage, vascular indentation (protrusion) and vascular process (bud-like process) were developed from intact venules at the wound margins. It is concluded that the formation of thrombus and terminal blind branch vessels constitute the initial reparative reactions of the injured vascular network and that new vessels then begin to form by outgrowth of protrusions and bud-like processes from intact venules at the wound margins.

Animals↗
PubMed1992

Involvement of putrescine in the development of kindled seizure in rats.

During the development of kindling by daily electrical stimulations applied to the left amygdala of rats, concentrations of the polyamines putrescine, spermidine, and spermine were measured in the left amygdala and the remainder of the cerebrum. A significant increase of putrescine concentration appeared first at the left amygdala in prekindled rats and then propagated to the remainder of the cerebrum with the development of kindling. This increase in putrescine concentration in the left amygdala was higher in prekindled rats than in fully kindled rats and lasted for at least 24 h after the final kindling stimulation. The concentrations of spermidine and spermine were slightly increased in a fully kindled state. To clarify the role of putrescine in kindling, the development of amygdaloid kindling was examined in rats after microinjections of alpha-difluoromethylornithine, a specific inhibitor of polyamine synthesis, and putrescine into the ipsilateral amygdala. Pretreatment with alpha-difluoromethylornithine (50 nmol) for 10 days accelerated both the development of behavioral kindling and the propagation of the afterdischarge from the left amygdala to the frontal cortex. In contrast, pretreatment with putrescine (200 nmol) for 10 days retarded the development of kindling. These results suggest that the increase in putrescine concentration in the kindled brain has an inhibitory effect on the development of kindling.

Amygdala↗
PubMed1992

Differential sensitivity of diabetic rat papillary muscles to negative inotropic effects of oxybarbiturates versus thiobarbiturates.

The negative inotropic effects of oxybarbiturates and thiobarbiturates were examined in papillary muscles isolated from streptozotocin-induced diabetic rats and in papillary muscles from age-matched control rats. The muscles from diabetic rats exhibited less negative inotropic responses to pentobarbital and secobarbital than the muscles from control rats. Conversely, the negative inotropic responses to thiopental and thiamylal were significantly enhanced in diabetic muscles. Differences in sensitivity to pentobarbital between control and diabetic muscles became less marked by treatment with ouabain or by lowering [Na+]o. Enhancement of the negative inotropic effect of thiamylal observed in diabetic muscles remained unchanged with these treatments. In both control and diabetic muscles, the negative inotropic effect of pentobarbital was completely reversed by increasing [Ca2+]o, but the effect of thiamylal was only partially reversed. These results suggest a difference in mechanism of action involved in establishment of the negative inotropic effects of oxybarbiturates vs thiobarbiturates. Oxybarbiturates appear to exclusively reduce the influx of extracellular Ca2+, whereas thiobarbiturates appear to affect Ca2+ movements at the Ca2+ storage sites in addition to the Ca2+ influx inhibition.

Animals↗
PubMed1992

Modes of the Na channel blocking action of pilsicainide, a new antiarrhythmic agent, in cardiac cells.

Using a whole cell clamp technique, the blockade of sodium currents (INa) by pilsicainide, a new antiarrhythmic agent, applied either intracellularly or extracellularly, was studied in single myocytes isolated from guinea pig right ventricle. Pilsicainide applied extracellularly inhibited the peak amplitude of INa in concentration- (from 10(-5) M to 10(-4) M) and rate- (from 0.5 Hz to 3.0 Hz) dependent manners. The onset rate of the blockade in INa was almost constant, independent of frequency of stimulus, but higher at high concentration of pilsicainide. The time constant in the recovery phase from INa inactivation remained almost constant (65 to 75 msec) in the range of concentrations used. Similar results were obtained by intracellular application of 10(-3) M pilsicainide. Pilsicainide applied intracellularly inhibited INa in a rate-dependent manner. The blocking potency of internally applied pilsicainide almost corresponded to that of external 10(-5) M pilsicainide. The onset rate of INa inactivation (from 0.098/pulse to 0.130/pulse) and the recovery time constant (77 msec) was similar to those of external 10(-5) M pilsicainide. These results suggest that pilsicainide, irrespective of intra- or extracellular application, shares a common binding site to block INa in cardiac myocytes.

Animals↗
PubMed1992

Effect of a phorbol ester on immunoreactive endothelin-1 release from cultured porcine aortic endothelial cells.

This study was designed to examine how protein kinase C (PKC) regulates the release of endothelin-1 (ET-1) from cultured porcine aortic endothelial cells. We measured the release of immunoreactive (IR)-ET-1 from cells cultured for up to 72 h in the presence or absence of a phorbol ester TPA. The release of IR-ET-1 from control cells (no TPA) increased according to time for up to 72 h. In the presence of TPA, the release of IR-ET-1 from the cells was higher than the control level for up to 8 h, but was lower thereafter and reached a plateau after 48 h. TPA dose-dependently stimulated IR-ET-1 release during incubation for 4 h, but suppressed it after incubation for 72 h. Stimulation of PKC by diacylglycerol mimicked the early (4 h) action of TPA. On the other hand, pretreatment of cells with TPA to downregulate PKC significantly suppressed basal and thrombin- or FCS-stimulated IR-ET-1 release. These findings suggest that the activation of PKC is related to the stimulation of ET-1 release and that down-regulation of PKC leads to the suppression of ET-1 release from cultured endothelial cells.

Animals↗
PubMed1992

Increased responses to adenosine and 2-chloroadenosine of cyclic AMP-generating systems in the primary cortical region of cobalt-induced epilepsy in the rat.

The epileptic activity was induced by an injection of cobalt chloride solution into the unilateral sensorimotor cortex of rats. Cyclic AMP accumulations elicited by adenosine and 2-chloroadenosine were investigated in slices from different regions of the epileptic cortex. The cyclic AMP accumulation was increased in the primary cortical region of cobalt-induced epilepsy. The greatest increase in cyclic AMP accumulation was detected between 2 and 3 weeks after treatment by cobalt, in conjunction with the electrographic and behavioral findings. The results suggest the functional significance of cortical cyclic AMP-generating systems in cobalt-induced epilepsy.

2-Chloroadenosine↗