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K Inoue

Publications and source records attributed to K Inoue.

At least 919 records · Page 51Linked to original sources
PubMed1997

Effects of fluvoxamine on food intake during rebound hyperphagia in rats.

We examined the effects of fluvoxamine on food intake during rebound hyperphagia induced by a time-restricted feeding schedule in rats. Rats were allowed access to food for only 2 h daily for 7 days, and then had free access to food for 7 consecutive days. The daily food intake of the rats was dramatically increased, by 42.5% (rebound hyperphagia), for 7 days of the free-feeding period. Intraperitoneal injection of fluvoxamine decreased food intake significantly in a dose-dependent manner for the first 3 h of feeding during 7 days. When rats were allowed access to one of the standard, carbohydrate-, fat-, or protein-rich diets in the free-feeding period following the time-restricted feeding schedule, fluvoxamine significantly decreased food intakes of standard, carbohydrate- and fat-rich diets on all days, and the protein-rich diet after the 2nd day of the free-feeding period. These results indicate that fluvoxamine, irrespective of the diet composition, suppresses rebound hyperphagia induced by a time-restricted feeding schedule, but that its effect is short-lived.

Animals↗
PubMed1997

Bromocriptine enhances feeding behavior without changing dopamine metabolism.

Bromocriptine is an ergot derivative and has been thought to act as a selective D2 receptor agonist, but its effects on dopamine release in vivo have not been confirmed. We administered bromocriptine into the striatum of rats and studied the effects on feeding behavior and dopamine release. Bromocriptine was perfused via a microdialysis probe into the ventrolateral striatum of rats fasted for 22 h, and the rats were then allowed to feed freely for 6 h. Bromocriptine perfusion increased food intake in a dose-dependent manner, whereas the extracellular concentrations of dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC), and homovanillic acid (HVA) did not change. Perfusion of (-) sulpiride, a selective D2 receptor antagonist, decreased food intake, but increased dopamine release and the levels of DOPAC and HVA. Pretreatment with (-)sulpiride perfusion for 1 h prior to bromocriptine perfusion inhibited the increase of food intake induced by bromocriptine, and it increased dopamine release and the levels of DOPAC and HVA. These findings suggest that bromocriptine directly perfused into the ventrolateral striatum acts selectively on postsynaptic D2 receptors and enhances feeding behavior.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1997

Pituitary folliculo-stellate-like cell line produces a cytokine-induced neutrophil chemoattractant.

In previous studies, we reported that cytokine-induced neutrophil chemoattractant (CINC) was produced in the pituitary gland. Here we investigated the possibility of detection of CINC immunoreactivity in the pituitary folliculo-stellate (FS)-like cell line (TtT/GF). Intense immunoreactivity was observed by immunocytochemistry in the cytoplasm and cell processes of TtT/GF cells. CINC immunoreactivity was detected by an enzyme-linked immunosorbent assay in as little as 3 h after conditioning the medium with TtT/GF cells, and it increased significantly in a time-dependent manner during the first 24 h of the culture. This immunoreactivity could be induced by lipopolysaccharide and tumor necrosis factor-alpha in a time- and dose-dependent manner. We also observed the expression of CINC mRNA in TtT/GF cells and LPS increased CINC mRNA accumulation in TtT/GF cells. These findings indicate that CINC produced by FS cells may play a role as a paracrine factor of the anterior pituitary gland, and TtT/GF will provide a useful model system for studying the regulation of CINC secretion by FS cells.

Animals↗
PubMed1997

Acute hepatitis caused by sexual or household transmission of GBV-C.

BACKGROUND/AIMS: Transfusion transmission is the only known transmission route of the recently identified GBV-C. To date, no evidence of household transmission of GBV-C has been reported. In the present study, a case of acute GBV-C hepatitis was investigated with respect to the mode of transmission. METHODS: A 24-year-old woman with acute GBV-C hepatitis and her asymptomatic husband were examined. Two GBV-C RNA samples, isolated at different times from both the patient and her husband were amplified by reverse transcriptase-polymerase chain reaction using sequences from the NS3 region. Sequencing of this region was subsequently performed for all four samples. RESULTS/CONCLUSIONS: The genomic RNA sequences of GBV-C isolated from each partner at two different time points were found to be 100% homologous. However, these genomic GBV-C RNA sequences differed in the NS3 (helicase) region from the genomic RNA isolated from the GBV-C prototype previously reported by Simons et al. Nonetheless, high homology (83%) was found between the GBV-C prototype and the GBV-C isolated from our patients. In addition, four nucleotides of the GBV-C RNA in the present study are unique and are not present in any other reported sequences of GBV-C. These results strongly suggest that GBV-C is one of the etiological agents involved in severe liver injury and was transmitted between this couple.

Acute Disease↗
PubMed1997

The differential osmoregulation and localization of taurine transporter mRNA and Na+/myo-inositol cotransporter mRNA in rat eyes.

We studied the cellular localization and osmotic regulation of taurine transporter (TauT) mRNA in the rat eyes using in situ hybridization. TauT mRNA signals were expressed in the ciliary body, and the outer part of the inner nuclear layer (INL), the outer nuclear layer (ONL) and the inner segment (IS) of the adult rat retina. Chronic hypernatrema, induced by gavaging with 1 ml/100 g body weight of 5% NaCl every other day for 7 days, markedly increased in TauT mRNA in the retina compared with control rats. However, there was little change in TauT mRNA in the eyes in acute hypernatremic state that is induced by single injection of high concentration of NaCl. On the contrary, acute hypernatremic rats displayed markedly elevated Na+/myo-inositol cotransporter (SMIT) mRNA in the retina and the iris-ciliary body and the lens epithelium. Under chronic hypernatremic conditions, there was no significant increase in SMIT mRNA in rat eyes. These findings suggest that TauT mRNA is osmotically regulated in vivo to protect retinal neuronal function, especially against chronic hypernatremic conditions, in contrast to rapid up-regulation of SMIT mRNA in acute hypernatremic rats.

Animals↗
PubMed1997

Analyses of extrathymic T cell differentiation in nu/nu mice by grafting embryonal organs.

Fetal (days 15 to 17) organs such as the small intestine, stomach and pancreas were engrafted under the renal capsules of athymic nude (nu/nu) mice to examine the capacity of these organs to induce the differentiation of T cells. Eight weeks after engraftment, the engrafted organs had differentiated into adult-type organs histologically. In the lamina propria of the engrafted small intestine, large intestine, and stomach, there were clusters of lymphocytes or lymphoid follicles, which included Thy1.2+ or CD4+ T cells. Flow cytometric analyses revealed that the lymphocytes from the lymph nodes of sham-, esophagus-, or pancreas-engrafted mice included very few T cells (1.20%), whereas those from the lymph nodes of the fetal small intestine-, large intestine-, or stomach-engrafted mice included significant numbers of T cells (8.36%) 8 weeks after engraftment, although there were not as many as in the fetal thymus-engrafted mice (17.97%). The peripheral T cells in the small intestine-, large intestine-, or stomach-engrafted mice were of bone marrow origin, and consisted of Thy1.2+, CD3+, and CD4+8-, or CD4-8+ with T cell receptor (TcR) alpha beta cells. Taken together, these findings indicate that not only the murine small intestine and large intestine but also the stomach have the capacity to induce the differentiation of T cells.

Animals↗
PubMed1997

The appearance of unusual phenotypic cells (CD4+ Mac-1+ class II+) in the liver of (NZW x BXSB)F1 mice is possibly an animal model for autoimmune hepatitis.

The male (NZW x BXSB)F1 (W/BF1) mouse, a murine model for autoimmune diseases, shows hepatosplenomegaly with lymphoid cell infiltration in the liver by 20 weeks of age. The majority of infiltrating cells are T cells, B cells and plasma cells, as seen in autoimmune hepatitis. Together with the increase in serum glutamate pyruvate transaminase (GPT) levels, anti-dsDNA antibody (Ab) and circulating immune complex (CIC) levels increase with age. These findings are compatible with those of autoimmune hepatitis in humans. In addition, a unique finding in this mouse is the accumulation of CD4+ Mac-1+ Class II+ cells in the sinusoidal space. The cells have the capacity to proliferate and differentiate into macrophages in vitro, indicating that they are the precursors of macrophages. This W/BF1 mouse provides a useful tool for not only analyzing the pathogenesis of autoimmune hepatitis but also establishing a new therapeutic strategy for it. In addition, we discuss the significance of the appearance of abnormal cells in autoimmune-prone mice.

Animals↗
PubMed1997

In vitro effects of sho-saiko-to on production of granulocyte colony-stimulating factor by mononuclear cells from patients with chronic hepatitis C.

During the past 2 years, drug-induced interstitial pneumonia was reported in 66 Japanese patients, mainly among chronic hepatitis C patients, undergoing treatment with the Japanese herbal medicine "Sho-saiko-to" (TJ-9). As interstitial pneumonia is also induced by granulocyte colony-stimulating factor (G-CSF), we examined the effects of TJ-9 on G-CSF production in peripheral blood mononuclear cells. In patients with hepatitis B or C, G-CSF production in the absence of any stimulation was significantly lower than healthy controls (p < 0.01). G-CSF production increased along with the increase of TJ-9 levels, and this could induce excessive production of G-CSF in hepatitis C patients, and this may be a cause of interstitial pneumonia.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1997

Intraoperative evaluation of small-calibre arterial reconstructions.

A new hammerhead-shaped, small probe for intraoperative duplex ultrasound was devised to evaluate small-calibre arterial reconstructions. This probe was used in two patients; one with terminal liver cirrhosis who had a left hepatic lobe that had been transplanted from her mother, and a second patient with limb-threatening ischaemia who had undergone arterial reconstructions. The technique was diagnostically useful and contributed to successful clinical outcomes.

Adolescent↗
PubMed1997

Positive correlation between prolonged potentiation of binding of double-stranded oligonucleotide probe for the transcription factor AP1 and resistance to transient forebrain ischemia in gerbil hippocampus.

Gel retardation electrophoresis revealed that binding of a radiolabelled double-stranded oligonucleotide probe for the nuclear transcription factor activator protein-1 was markedly potentiated in the CA1 and CA3 subfields and the dentate gyrus of the hippocampus of the gerbils with transient forebrain ischemia for 5 min, which is known to induce delayed death of pyramidal neurons exclusively in the CA1 subfield. The potentiation was transient in the vulnerable CA1 subfield, but persistent up to 18 h in the resistant CA3 subfield and dentate gyrus. However, no significant alteration was detected in endogenous levels of cyclic AMP response element binding protein phosphorylated at serine133 in these three different hippocampal structures 3 h after the reperfusion. On the other hand, hypothermia during ischemia which is known to protect the CA1 subfield against ischemic damages, led to a prolonged elevation of the activator protein-1 binding up to 9 h after the reperfusion in this vulnerable subfield at least in part through expression of c-Fos protein. Moreover, activator protein-1 binding was significantly elevated in the CA1 subfield up to 12 h after forebrain ischemia for 2 min which is shown not to induce marked damages to the vulnerable subfield. These results suggest that prolonged elevation of DNA binding activity of activator protein-1 may be responsible for molecular mechanisms underlying the unique vulnerability and/or resistance of particular subfields to a transient ischemic insult in the gerbil hippocampus.

Adaptor Protein Complex 1↗
PubMed1997

Interaction of goosecoid and brachyury in Xenopus mesoderm patterning.

Detailed in situ analyses reveal overlapping expression of gsc and Xbra in the early Spemann's organizer. Coexpression is lost during gastrulation suggesting an interaction between these genes. Ectopic expression of gsc ventrally suppresses endogenous Xbra expression and transcription from Xbra promoter reporter gene constructs. Suppression is mediated, at least partially, by a gsc-binding site within the first 349 bp of the promoter. Xbra reporter gene transcription is also suppressed in the region of endogenous gsc expression, whereas high-level ectopic Xbra expression has no effect on endogenous gsc expression. We suggest that early patterning of the vertebrate mesoderm, like early patterning of the Drosophila embryo, occurs by first establishing broad domains of gene expression which are subsequently refined by intergenic interactions to further delimit tissue boundaries.

Animals↗
PubMed1997

Azelastine suppresses the release of arachidonic acid metabolites from cultured human umbilical vein endothelial cells.

We investigated the effects of azelastine, an anti-allergic agent, on the release of arachidonic acid metabolites from cultured human umbilical vein endothelial cells (HUVEC). High performance liquid chromatography (HPLC) revealed that HUVEC treated with 10(-5) M azelastine released smaller amounts of arachidonic acid metabolites into the medium than control HUVEC. Azelastine significantly reduced the release of prostaglandin F2 alpha (PGF2 alpha), leukotriene B4 (LTB4) and 5-hydroxy-eicosatetraenoic acid (5-HETE) by HUVEC. These results suggest that azelastine may inhibit contraction of bronchial smooth muscle cells and reduce bronchial inflammation by suppressing the release of arachidonic acid metabolites from vascular endothelial cells.

Anti-Allergic Agents↗
PubMed1997

Modulation of doxorubicin resistance in a doxorubicin-resistant human leukaemia cell by an immunoliposome targeting transferring receptor.

Using a doxorubicin-resistant subline (K562/ADM) of human leukaemia K562 cells (Tsuruo et al, 1986), the effect of immunoliposomes that targeted a cellular transferrin receptor (TFR) was examined by neutralization of doxorubicin (DOX) resistance. OKT9-CIL, prepared by conjugation of DOX-encapsulated liposome with an anti-TFR monoclonal antibody, OKT9 (Aisenberg and Wilkes, 1980), showed similar binding to both K562 and K562/ADM. Although an 80-fold higher sensitivity to free DOX on cell growth inhibition in K562 than in K562/ADM was found, the difference was clearly diminished after OKT9-CIL treatment through the increased sensitivity of K562/ADM. The cellular DOX level 30 min after the exposure of free DOX was 45-fold lower in K562/ADM than in K562, whereas nearly equivalent DOX levels were detected in K562 and K562/ADM after OKT9-CIL treatment. In addition, DOX in K562/ADM in the free DOX treatment was efficiently excreted by 54% within 120 min of incubation, whereas almost all DOX supplied by OKT9-CIL remained uncleared. Fluorescence microscopic observation showed that OKT9-CIL was internalized into juxtanuclear vesicles in K562/ADM cells. These results suggest that OKT9-CIL has a potency to accumulate DOX, resulting in augmentation of DOX cytotoxicity in DOX-resistant tumour cells.

Antibodies, Monoclonal↗
PubMed1997

Blockade of N-type Ca2+ current by cilnidipine (FRC-8653) in acutely dissociated rat sympathetic neurones.

1 The inhibitory effects of cilnidipine (FRC-8653) and various organic Ca2+ channel blockers on high voltage-activated Ba2+ currents (HVA IBa) in rat sympathetic neurones were examined by means of the conventional whole-cell patch-clamp recording mode under voltage-clamped conditions. 2 HVA IBa was classified into three different current components with subtype selective peptide Ca2+ channel blockers. No omega-Agatoxin IVA-sensitive (P-type) or omega-conotoxin MVIIC-sensitive (Q-type) current components were observed. Most (> 85%) IBa was found to consist of omega-conotoxin GVIA-sensitive N-type components. 3 The application of cilnidipine inhibited HVA 1Ba in a concentration-dependent manner. The Kd value for cilnidipine was 0.8 microM. Cilnidipine did not shift the current-voltage (I-V) relationship for HVA IBa, as regards the threshold potential and peak potential where the amplitude reached a maximum. 4 High concentration of three hypotensive Ca2+ channel blockers, nifedipine, diltiazem and verapamil, all inhibited HVA IBa in a concentration-dependent manner. The Kd values for nifedipine, diltiazem and verapamil were 131, 151 and 47 microM, respectively. A piperazine-type Ca2+ channel blocker, flunarizine, showed a relatively potent blocking action on IBa. The Kd value was about 3 microM. 5 These results thus show that cilnidipine potently inhibits the sympathetic Ca2+ channels which predominantly consist of an omega-Cg-GVIA-sensitive component. This blockade of the N-type Ca2+ channel, as well as the L-type Ca2+ channel by cilnidipine suggests that it could be used therapeutically for treatment of hypersensitive sympathetic disorders associated with hypertension.

Animals↗
PubMed1997

Inhibition by ATP of calcium oscillations in rat cultured hippocampal neurones.

1 The effect of adenosine 5'-triphosphate (ATP) on glutamatergic synaptic transmission in hippocampus was examined by an indicator of intracellular Ca2+ oscillations. These oscillations were postsynaptic responses by glutamate released from presynaptic sites. ATP completely inhibited the oscillations in a concentration-dependent manner. 2 The ATP-induced inhibition was mediated via P2-purinoceptors since ATP exhibited the inhibitory action even in the presence of P1-purinoceptor antagonists. Also non-hydrolysable ATP analogues and uridine 5'-triphosphate (UTP) inhibited the oscillation. 3 The rank order of agonist potency of ATP analogues for inhibition of the Ca2+ oscillation was as follows: 2-methyl-thio-adenosine 5'-triphosphate > or = ATP > adenosine 5'-O-(3-thiotriphosphate)>UTP> alpha, beta-methylene-adenosine 5'-triphosphate. These inhibitory effects were insensitive to suramin. Judging from this rank order of potency, the inhibitory P2-purinoceptor could be assigned to a subclass of GTP-binding protein coupled-type receptors. 4 The site of action of ATP was thought to be presynaptic since ATP did not affect the postsynaptic Ca2+ responses by glutamate. These results suggest the existence of a presynaptic inhibitory P2-receptor that inhibits glutamate release in the hippocampus.

Adenosine Triphosphate↗
PubMed1997

Potent and voltage-dependent block by philanthotoxin-343 of neuronal nicotinic receptor/channels in PC12 cells.

1. Block by philanthotoxin-343 (PhTX-343), a neurotoxin from wasps, of ionic currents mediated through neuronal nicotinic acetylcholine (ACh) receptor/channels was characterized in rat phaeochromocytoma PC12 cells, by use of whole cell voltage-clamp techniques. 2. In the cells held at -60 mV, PhTX-343 at 0.1 and 1 microM inhibited an inward current activated by 100 microM ACh. The current inhibition was relieved by depolarizing steps, and augmented at negative potentials, suggesting that PhTX-343 blocks the channel in a voltage-dependent manner. Joro spider toxin-3 (JSTX-3) also exerted voltage-dependent inhibition of ACh-activated currents in a similar concentration range, but argiotoxin636 did not affect the currents. 3. Analysis of the current decay during hyperpolarizing steps indicated that the current inhibition by 100 nM PhTX-343 develops in an order of several hundres of milliseconds. On the other hand, the recovery from the current inhibition during depolarizing steps developed in an order of about 100 ms. 4. The results suggest that PhTX-343 blocks neuronal nicotinic receptor channels in PC12 cells at concentrations lower than those required for channel block in non-mammalian cells, and the block exhibits clear voltage-dependence. Estimated from the voltage-dependence, the binding site of PhTX-343 may be located near the outer mouth of the channel.

Acetylcholine↗