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Biomedical subjects

Y Kataoka

Publications and source records attributed to Y Kataoka.

At least 37 records · Page 2Linked to original sources

Gonadal regulation of PrRP mRNA expression in the nucleus tractus solitarius and ventral and lateral reticular nuclei of the rat.

We investigated the prolactin-releasing peptide (PrRP) gene expression quantitatively in the rat brain and the involvement of estrogen and progesterone using in situ hybridization. The strongest signals were observed in the nucleus tractus solitarius (NTS), which showed approximately 70% of total PrRP mRNA in the brain. Moderate expression was observed in the ventral and lateral reticular nuclei (VLRN) of the medulla oblongata. PrRP mRNA signals in the hypothalamic ventromedial- and dorsomedial nuclei showed only 5% of total signals. The PrRP mRNA expression among female rats showing normal gonadal cycle and male rats showed that the highest levels were in female rats in proestrus. Administration of estrogen or progesterone after ovariectomy induced an increase in PrRP mRNA expression in the NTS. PrRP mRNA content in the NTS increased with the progress of the pregnancy and reached a peak on the 14th day, the mid-period of pregnancy, when plasma progesterone increases. We also observed the colocalization of PrRP and estrogen receptor alpha in the neurons distributed in the NTS by double labeling immunocytochemistry. These findings indicate that PrRP gene expression is regulated by gonadal steroid hormones in the medulla oblongata, and parts of PrRP synthesizing neurons are considered to be directly influenced by estrogen in the NTS.

Animals↗

Abnormalities of synapses and neurons in the hippocampus of neuropsin-deficient mice.

In the present study, we produced null-mutant mice of neuropsin, an extracellular matrix serine protease, to examine the neural functions of this protein particularly in the hippocampus. Golgi-Cox impregnation and Nissl-staining revealed morphological change of cell soma in the mutant mice compared to wild-type mice. However, Golgi-Cox impregnation revealed no apparent change in the dendritic arborization and spine density. Quantitative electronmicroscopic analysis revealed that number of asymmetrical synapses were significantly decreased in the stratum radiatum, the major terminal field of Schaffer-collaterals, whereas free boutons still holding synaptic vesicles but with no synaptic specialization were increased in number in the same microscopic fields. An increased number of parvalbumin-immunoreactive cells (known as fast spiking cells) in mutant was also observed. These results strongly suggest that neuropsin is involved in connectivity of a group of CA1 synapses and consequently in the hippocampal networking.

Animals↗

Morphologic degeneration of human microvascular endothelial cells induced by iodinated contrast media.

RATIONALE AND OBJECTIVES: The purpose of this study was to characterize the adverse effects of iohexol and ioxaglate on human microvascular endothelial cells, which may result in phlebitis, pain, and thrombosis. MATERIALS AND METHODS: The degree of morphologic degeneration and of lactate dehydrogenase (LDH) efflux into the extracellular medium (as an index of cell viability) were determined in endothelial cell culture exposed for 10, 30, or 60 minutes to ioxaglate or iohexol (ionic and nonionic contrast media, respectively) at iodine concentrations of 100 or 150 mg/mL. RESULTS: Ioxaglate induced concentration- and time-dependent morphologic degeneration, including shrinkage and loss of the cell tip in 20%-80% of endothelial cells; iohexol did not. After 60 minutes of exposure, ioxaglate at the higher concentration (150 mg iodine per milliliter) significantly increased the LDH signal (ie, the percentage of LDH released), to 20%. CONCLUSION: The present findings demonstrate that ioxaglate but not iohexol causes morphologic degeneration of the microvascular endothelial cells. This direct cytotoxic action of ioxaglate probably causes endothelial cell dysfunction, closely associated with the occurrence of phlebitis, pain, and thrombosis.

Cells, Cultured↗

Developmental roles and molecular characterization of a Drosophila homologue of Arabidopsis Argonaute1, the founder of a novel gene superfamily.

BACKGROUND: Arabidopsis Argonaute1 (AGO1) is the founder of a novel gene superfamily that is conserved from fission yeasts to humans. AGO1, and several other members of this superfamily are necessary for stem cell renewal or RNA interference. However, little has been reported about their roles in animal development or about the molecular activities of any of the members. RESULTS: We have isolated a Drosophila homologue of AGO1, dAGO1, in our attempt to search genetically for regulators of Wingless (Wg) signal transduction. dAGO1 is broadly expressed in the embryo and the imaginal disc. dAGO1 over-expression at wing margins suggested that it behaves as a positive regulator in the genetic background employed. Loss-of-function mutations of dAGO1, unexpectedly, did not give typical segment polarity phenotypes of the wg class; instead, dAGO1 maternal and zygotic mutant embryos showed developmental defects, with malformation of the nervous system being the most prominent. The mutant decreased in the numbers of several types of neurones and glia examined. The dAGO1 protein was distributed in the cytoplasm and co-sedimented with poly(U)- or poly(A)-conjugated beads. CONCLUSION: Our results suggest that the dAGO1 protein exerts its developmental functions by binding to RNA either directly or indirectly.

Amino Acid Sequence↗

The role of donor T cells for target organ injuries in acute and chronic graft-versus-host disease.

Donor T cells are crucial for target organ injury in graft-versus-host disease (GVHD). We examined the effects of donor T cells on the target organs using a parent-into-F1 model of acute and chronic GVHD. Donor T cells showed engraftment in the spleen, small intestine and liver of mice with acute GVHD, causing typical GVHD pathology in these organs. Interferon-gamma and Fas ligand expression were up-regulated, and host lymphocytes were depleted in the target organs of these mice. In contrast, donor T cells did not show engraftment in the small intestine of mice with chronic GVHD, and no GVHD pathology was observed in this organ. However, both donor T-cell engraftment and GVHD pathology were observed in the spleen and liver of chronic GVHD mice, along with the up-regulation of interleukin-4 (IL-4) and IL-10 expression plus the expansion of host lymphocytes such as splenic B cells and hepatic natural killer (NK) 1.1+ T cells. Donor anti-host cytotoxic T-lymphocyte activity was observed in spleen cells from mice with acute GVHD, but not in spleen cells from mice with chronic GVHD. Transplantation of Fas ligand-deficient (gld) spleen cells did not induce host lymphocyte depletion in target organs. These results indicate that donor T cells augment type 1 T helper immune responses and deplete the host lymphocytes from target organs mainly by Fas-mediated pathways in acute GVHD, while donor T cells augment type 2 T helper immune responses and expand host splenic B cells and hepatic NK1.1+ T cells in chronic GVHD.

Acute Disease↗

Particulate contamination of lyophilized amphotericin B preparation during reconstitution process.

OBJECTIVE: To investigate the effect of the reconstitution methods for the commercial amphotericin B preparation with respect to particulate contamination. METHODS: The particle counts in amphotericin B solutions reconstituted according to three different methods and amphotericin B fluids made with intravenous fluids after reconstitution were performed using a light extinction method. The particle contaminants were identified with X-ray emission spectrometry attached to a scanning electron microscope. RESULTS: Amphotericin B in a vial induced particle contamination during the reconstitution process, and the contamination was especially marked by shaking vigorously after injecting water into the vial. From the X-ray analysis, it appeared that the increased number of particles was derived from the amphotericin B-deoxycholate complex containing substances such as silicone released from the vial components. Amphotericin B fluid made with intravenous fluids after reconstitution also contained particles over the acceptable limits according to the Japanese or US pharmacopoeia. CONCLUSION: These findings suggest that reconstituted solutions should be filtered with membrane filters and diluted fluids with in-line filters.

Amphotericin B↗

A leucine(7)-to-proline(7) polymorphism in the signal peptide of neuropeptide Y was not identified in the Japanese population.

OBJECTIVE: A Leu(7)-to-Pro(7) polymorphism exists in the signal peptide part of prepro-neuropeptide Y (NPY) and this polymorphism is associated with high serum cholesterol and LDL cholesterol levels in both Finnish and Dutch people. There was a significant difference in the allelic frequencies among populations with different genetic backgrounds. Therefore, the present study was designed to test whether Japanese people had the Leu(7)-to-Pro(7) polymorphism in the NPY signal peptide. METHODS: A total of 102 healthy Japanese volunteers supplied blood samples, from which leucocyte DNA was isolated. Primer pairs for the polymerase chain reaction (PCR) were made according to Karvonen et al. Direct sequencing of the PCR product was carried out by the dye terminator method using a capillary electrophoresis sequencer. RESULTS: All 102 young healthy Japanese subjects showed Leu(7)/Leu(7) but not Leu(7)/Pro(7) or Pro(7)/Pro(7) in the NPY signal peptide. CONCLUSION: The incidence of the Leu(7)-to-Pro(7) polymorphism in the signal peptide of NPY was extremely low in Japanese people, suggesting that the polymorphism producing Pro(7) is not one of the genetic determinant factors affecting serum cholesterol levels in Japanese people.

Adult↗

Microanalysis of propofol in human serum by semi-microcolumn high-performance liquid chromatography with UV detection and solid-phase extraction.

OBJECTIVE: To develop a simple analytical method for monitoring the low serum levels of propofol found when administered for the sedation of patients in the intensive care unit (ICU). METHODS: A high-performance liquid chromatographic method (HPLC) was used with UV detection. Solid-phase extraction (SPE) cartridges and a semi-microcolumn (TSK gel ODS-80Ts, 2.0 mm i.d. x 25 cm, 5 microm) were used to improve sensitivity. Propofol in the eluate obtained from the SPE cartridge was concentrated to about five times the initial concentration. RESULTS: The sensitivity using the semi-microcolumn was amplified by about three-fold. The assay showed a good linearity with a quantification limit 20 ng/mL. Intra- and inter-assay coefficients of variation were less than 2.2% and 10.0%, respectively. The mean recoveries ranged from 97.6 to 109.5%. CONCLUSION: The HPLC method described should be useful for measuring the low serum propofol levels found when the drug is used for ICU sedation.

Chromatography, High Pressure Liquid↗

Contrast medium-induced pulmonary vascular hyperpermeability is aggravated in a rat climacterium model.

UNLABELLED: Tominaga K, Kataoka Y, Sendo T, et al. Contrast medium-induced pulmonary vascular hyperpermeability is aggravated in a rat climacterium model. Invest Radiol 2001;36:131-135. RATIONALE AND OBJECTIVES: To test whether climacterium influences adverse pulmonary reactions to contrast media, the authors investigated the effect of ioxaglate on pulmonary vascular permeability in ovariectomized rats as a climacterium model. METHODS: From 7 days after surgery, ovariectomized rats were treated with estradiol valerate or vehicle once per week for 3 weeks. At 28 days after surgery, ioxaglate, an ionic contrast medium, was intravenously injected at 1.5 mL/min in rats. Pulmonary vascular permeability was evaluated by measuring the amount of Evans blue dye in the lung tissue. RESULTS: Ioxaglate dose-dependently increased pulmonary vascular permeability in sham-operated and ovariectomized rats. Ovariectomized rats showed a 2.6-fold increased aggravation of vascular permeability by ioxaglate 4 g I/kg compared with sham-operated rats. Estradiol valerate (0.2-5.0 mg/kg) dose-dependently blocked ioxaglate-increased vascular permeability in ovariectomized rats. CONCLUSIONS: These findings suggest that climacterium is included, at least in part, in the risk factors for contrast-induced adverse pulmonary reactions, and this risk is lowered by estrogen replacement therapy.

Animals↗

Hepatocyte growth factor ameliorates acute graft-versus-host disease and promotes hematopoietic function.

Acute graft-versus-host disease (GVHD) is a major complication of bone marrow transplantation (BMT) and is characterized by hematopoietic dysfunction, immunosuppression, and tissue injury in the skin, liver, and intestinal mucosa. Hepatocyte growth factor (HGF), originally identified and cloned as a potent mitogen for hepatocytes, induces mitogenic and antiapoptotic activity in various epithelial cells and promotes hematopoiesis. Working in a murine model of acute GVHD, we performed repeated transfection of the human HGF cDNA into skeletal muscle and showed that this treatment inhibited apoptosis of intestinal epithelial cells and donor T-cell infiltration into the liver, thereby ameliorating the enteropathy and liver injury caused by acute GVHD. HGF also markedly suppressed IFN-gamma and TNF-alpha expression in the intestine and liver and decreased the serum IL-12. Furthermore, extramedullary hematopoiesis by donor cells was increased, and the survival rate was improved. These results suggest that HGF may be useful for controlling acute GVHD after allogeneic BMT.

Animals↗

A novel function of prolactin-releasing peptide in the control of growth hormone via secretion of somatostatin from the hypothalamus.

The present study examined a novel function of PRL-releasing peptide (PrRP) on the neuroendocrine. PrRP-immunoreactive nerve fibers and nerve terminals were located in the vicinity of the somatostatin (SOM)-neurons in the hypothalamic periventricular nucleus (PerVN). Immuno-electron microscopy revealed that PrRP-immunoreactive nerve terminals made synaptic contacts with nonimmunoreactive neuronal elements in the PerVN. Intracerebroventricular (icv) administration of PrRP induced immediate early gene, NGFI-A, in SOM-neurons in the PerVN. Double-labeling in situ hybridization showed that some parts of SOM-neurons in the PerVN expressed PrRP receptor messenger RNA. Therefore, some parts of SOM-neurons in the PerVN are considered to be directly innervated by PrRP via PrRP receptor. In addition to the above morphological characteristics, icv administration of PrRP decreased plasma GH levels. Such inhibitory effects of PrRP on the secretion of GH from the anterior pituitary were diminished by depletion or neutralization of SOM. From these findings it was strongly suggested that SOM-neurons respond to PrRP and secrete SOM into the portal vessels and thus inhibit GH secretion from the anterior pituitary.

Animals↗

Reversal of vinblastine resistance in human leukemic cells by haloperidol and dihydrohaloperidol.

Haloperidol, an antipsychotic, was investigated in cells overexpressing P-glycoprotein to detemine whether it was a clinically effective drug to reverse for reversing multidrug resistance (MDR) mediated by P-glycoprotein. A nontoxic concentration of haloperidol (1-30 microM) enhanced the cytotoxic effects of vinblastine (VBL) concentration-dependently in VBL-resistant human leukemia (K562/VBL) cells, but had no effect in the parent cells. Haloperidol also enhanced the cytotoxicities of epirubicin, doxorubicin and actinomycin D in the K562/VBL cells, but not those of idarubicin or cisplatin; this enhancement was less than that of the VBL toxicity in the VBL-resistant tumor line. Haloperidol increased the intracellular accumulation of VBL in the K562/VBL cells, and the binding of [3H]-azidopine to the cell-surface protein, P-glycoprotein, was inhibited by haloperidol in a concentration-dependent manner. Haloperidol was less potent than verapamil. Thus, haloperidol appeared to potentiate anticancer agents through the reversal of MDR by competitively inhibiting drug-binding to P-glycoprotein. In contrast, the main metabolite of haloperidol, dihydrohaloperidol, without antipsychotic activity, had less of an effect. Therefore, haloperidol might be useful in reversing drug-resistance.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

Acidosis inhibits gallbladder contraction mediated by protein kinase C activation.

The effects of extracellular acidosis on gallbladder contraction were investigated using gallbladder strips isolated from guinea pigs. In an acidic medium (pH 6.9), gallbladder contraction induced by histamine and prostaglandin E2 was significantly lower than that in a normal medium (pH 7.4). Acidosis affected neither gallbladder contraction induced by histamine in the absence of extracellular Ca2+ nor that induced by KCl. Acidosis significantly inhibited Ca2+-induced contraction in the presence of sodium fluoride and phorbol 12,13-dibutyrate but not that in the presence of KCl. Staurosporine (30 nM) significantly inhibited gallbladder contraction induced by histamine and prostaglandin E2, but not that by KCl. Histamine-induced contraction in the presence of staurosporine was not affected by acidosis. Acidosis significantly inhibited Ca2+-induced contraction in the presence of histamine but not that in the presence of both histamine and staurosporine. These results suggest that extracellular acidosis selectively inhibits gallbladder contraction mediated by protein kinase C activation.

Acidosis↗

Radiosensitivity of mammalian cell lines engineered to overexpress cytosolic glutathione peroxidase.

Reactive oxygen species are believed to be involved in radiation lethality. Glutathione peroxidase is an intracellular enzyme with antioxidant functions. To determine whether increasing the cellular antioxidant capacity can confer radiation resistance, the effect of overexpression of glutathione peroxidase on radiosensitivity was determined in two different cell types. An expression construct including the bovine cytosolic glutathione peroxidase cDNA was used to overexpress this enzyme in cells of the human lymphoblast cell line Sup-T1 as well as the Chinese hamster ovary cell line AA8. Supplementation of the culture media with 30 nM sodium selenite was included to obtain optimal glutathione peroxidase activity. Northern blot analysis confirmed the presence of the construct mRNA, and a standard coupled spectrophotometric assay demonstrated significantly increased glutathione peroxidase activity in the transfected cell lines. An approximately 8-fold increase was found in the Sup-T1 cells, and an approximately 30-fold increase was obtained in the Chinese hamster ovary AA8 cells. Clonogenic survival was assayed in the overexpressing cells and compared to that in control cells transfected with vector alone. Despite significantly increased glutathione peroxidase activity, no observable radioprotection was conferred in either of the two cell lines studied, indicating that increased glutathione peroxidase activity is insufficient to confer radioresistance in the two cell types examined. These data are discussed in the context of using antioxidants as adjuncts to clinical radiotherapy.

Animals↗

Severe fenitrothion poisoning complicated by rhabdomyolysis in psychiatric patient.

Non-traumatic rhabdomyolysis associated with organophosphate intoxication has not been generally reported. We report here in a severe case of fenitrothion poisoning complicated by rhabdomyolysis. A 43-year-old woman ingested approximately 100 ml of fenitrothion emulsion (50%) in an attempt to commit suicide. On day 3 after admission, her creatine phosphokinase (CPK) peaked at 47,762 IU/L. She received supportive treatment included sodium bicarbonate and fluid resuscitation. However, muscarinic symptoms including excessive miosis and salivation developed on day 5 when her CPK levels decreased. The delay in cholinergic symptoms might have been due to the trihexyphenidyl she took with the antipsychotic drugs. Fortunately, the present patient recovered from the acute cholinergic crisis, and acute renal failure was prevented by early diagnosis. This is a case of organophosphate poisoning complicated by rhabdomyolysis in a psychiatric patient. The masking of acute cholinergic symptoms should be taken into consideration in such patients.

Adult↗

[A frequent fiber-scopic bronchial lavege for the case of bilateral sever pulmonary contusion with flail chest].

A 26-year-old man was injured in the traffic accident. He had complicated chest trauma. He came to our hospital by ambulance immediately after rescued from crashed his automobile. He had severe pulmonary contusion with frail chest, pulmonary laceration, tension hemopneumothorax, and hypovolemic shock, and air embolism of the brain. He was managed with fiber-optic bronchoscopy under mechanical ventilation and chest drainage. Frequent broncho-scopic bronchial lavage of respiratory tract with thrombin and adrenaline solution was helpful to prevent anoxia due to complicated chest injury. He developed acute bacterial empyema and multiple organ failure due to septic shock during intensive care for trauma. However, he underwent surgical treatment for empyema and fully returned to his work after 6 months after his critical accident.

Accidents, Traffic↗

Case report: right subclavian artery pseudoaneurysm due to perforation of esophageal cancer.

A 51-year-old man presented with massive hematemesis. Perforation of upper esophageal cancer, which had already occurred at least six days earlier, progressed to upper mediastinitis. The mediastinitis contiguous to the right subclavian artery was considered to have caused a pseudoaneurysm. Rupture of the pseudoaneurysm into the esophagus resulted in massive hematemesis. Both enhanced computed tomography and angiography were diagnostic for the pseudoaneurysm. Transluminal endovascular stent-grafts placement was successful in preventing subsequent hemorrhage.

Aneurysm, False↗

Cyclosporine enhances alpha1-adrenoceptor-mediated nitric oxide production in C6 glioma cells.

The present study was aimed at elucidating the effect of cyclosporine on phenylephrine-evoked nitric oxide (NO) production in C6 glioma cells using direct electrochemical NO monitoring. Phenylephrine (0.1-10 microM) dose-dependently stimulated NO production (0.8-12.9 microM) and this was blocked by NO synthase inhibitor, prazosin, Ca2+-depletion and Xestospongin C (a blocker of the inositol 1,4,5-trisphosphate (IP3) receptor), suggesting that the alpha1-adrenoceptor signaling pathway mediates NO production in C6 cells. Cyclosporine (approximately 10 microM) failed to evoke NO production but increased phenylephrine-evoked NO production by 20-120% of phenylephrine alone in a dose-dependent manner (1-5 microM). Xestospongin C, at a concentration which showed no effect on phenylephrine-induced NO production, significantly inhibited the cyclosporine-enhanced phenylephrine response. This finding suggests that cyclosporine may increase phenylephrine-induced NO production by accelerating IP3 receptor function in the alpha1-adrenoceptor signaling pathway in C6 cells. This enhanced NO production in glial cells may be operative for the occurrence of cyclosporine neurotoxicity including convulsions and encephalopathy.

Adrenergic alpha-Agonists↗