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Search Results: 1 - 10 of 2020 matches for " Keiko Ueda "
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Hemoglobin Level Stability after a Switch from Darbepoetin Alfa to Epoetin Beta Pegol for the Treatment of Renal Anemia in Hemodialysis Patients  [PDF]
Sayaka Takahashi, Yoshiko Tanaka, Mari Takano, Keiko Suzuki, Mio Ueda, Yukiko Shimamoto, Kosaku Nitta
International Journal of Clinical Medicine (IJCM) , 2015, DOI: 10.4236/ijcm.2015.69087
Abstract: Background: New erythropoiesis-stimulating agents (ESAs) with a longer half-life have been developed for the treatment of anemia as a complication of patients with end-stage renal disease. Objectives: The objective of the present study was to assess the hemoglobin (Hb) stability of a Japanese cohort of hemodialysis (HD) patients who were simultaneously switched from darbepoetin alfa (DA) to epoetin beta pegol (CERA). Methods: This was an observational, prospective study of HD patients 20 years of age or more who were switched from intravenous (IV) DA to IV CERA and continued on HD for at least 3 months. The dose was adjusted to maintain the Hb level to within 1.0 g/dl of the baseline value. Results: A total of 68 HD patients (75.0% male, median age 63.0 years) were enrolled. The patients’ mean Hb levels were 10.8 ± (0.6) g/dl at Month 0, 10.9 ± 0.7 at Month 1, 10.8 ± 0.7 at Month 2, and 10.9 ± 0.8 at Month 3, and the differences from the level at Month 0 were not significant. After the switch, the ESA dose decreased significantly (P < 0.0001) from an annual mean DA dose of 549.0 ± 246.6 IU/kg/month to a mean CERA dose at Month of 3 491.0 ± 291.7 IU/kg/month. The ESA resistance index (ERI) decreased from 51.7 ± 24.4 IU/kg/ month/g/dl on DA at Month 0 to 46.4 ± 29.3 on CERA at 3 Month 3 (P < 0.0001). Conclusion: Switching from DA to CERA was associated with approximate 89% reduction of the required dose in Japanese HD patients being treated with an ESA and showed a favorable impact on the treatment of renal anemia, including the need for less frequent injections and a reduction of the ESA dose.
Clinical and Pathological Roles of Ro/SSA Autoantibody System
Ryusuke Yoshimi,Atsuhisa Ueda,Keiko Ozato,Yoshiaki Ishigatsubo
Clinical and Developmental Immunology , 2012, DOI: 10.1155/2012/606195
Abstract:
Clinical and Pathological Roles of Ro/SSA Autoantibody System
Ryusuke Yoshimi,Atsuhisa Ueda,Keiko Ozato,Yoshiaki Ishigatsubo
Journal of Immunology Research , 2012, DOI: 10.1155/2012/606195
Abstract: Anti-Ro/SSA antibodies are among the most frequently detected autoantibodies against extractable nuclear antigens and have been associated with systemic lupus erythematosus (SLE) and Sj?gren's syndrome (SS). Although the presence of these autoantibodies is one of the criteria for the diagnosis and classification of SS, they are also sometimes seen in other systemic autoimmune diseases. In the last few decades, the knowledge of the prevalence of anti-Ro/SSA antibodies in various autoimmune diseases and symptoms has been expanded, and the clinical importance of these antibodies is increasing. Nonetheless, the pathological role of the antibodies is still poorly understood. In this paper, we summarize the milestones of the anti-Ro/SSA autoantibody system and provide new insights into the association between the autoantibodies and the pathogenesis of autoimmune diseases. 1. Introduction Systemic autoimmune diseases, including systemic lupus erythematosus (SLE) and Sj?gren’s syndrome (SS), are a category of medical conditions that affects multiple organs and are related to autoimmune responses. These are commonly characterized by the development of autoantibodies against intracellular autoantigens. In fact, diagnosis, classification, and prognosis often rely on specificity and levels of the autoantibodies, in addition to clinical symptoms and other laboratory evaluations. Among autoantigens, extractable nuclear antigens (ENA) are soluble cytoplasmic and nuclear components with over 100 different antigens described. The main antigens used in immunological laboratories for detection are Ro, La, Sm, RNP, Scl-70, and Jo1 [1]. Anti-Ro/SSA and anti-La/SSB antibodies are among the most frequently detected autoantibodies against ENA and have traditionally been associated with SLE, SS, subacute cutaneous lupus erythematosus (SCLE), and neonatal lupus erythematosus (NLE) [2–5]. Anti-Ro/SSA and anti-La/SSB can be detected in 70–100% and 40–90%, respectively, of patients with SS [6], and the presence of these autoantibodies is one of the criteria for the diagnosis and classification of SS [7, 8]. Anti-Ro/SSA and anti-La/SSB antibodies were originally described in 1961 as two precipitating antibodies reacting with antigens contained in extracts from salivary and lacrimal glands of patients with SS, termed SjD, and SjT, respectively [9]. SjD antigen was reported to be insensitive to trypsin or heat, while SjT antigen could be destroyed by the same treatment. In 1969, Clark et al. described the presence of antibodies in the sera of patients with SLE that reacted with
Chromosomal Studies of Masculinized Hybrids in Bitterlings (Teleostei: Cypriniformes: Acheilognathinae)  [PDF]
Takayoshi Ueda, Yukie Ueda
Natural Resources (NR) , 2016, DOI: 10.4236/nr.2016.76028
Abstract: The chromosome analysis of the masculinized hybrid between female Tanakia limbata and male T. signifer in bitterlings (Acheilognathinae) was done. It was presumed that they had intermediate karyotype between the parents, and formed sperms with heteroploidy resulting from the incomplete pairing of homologous chromosomes in meiosis. Due to the abundance of species and the ease of artificial fertilization, the study of the factor of the hybrid sterility in bitterlings would lead to the clarification of the mechanism about species differentiation and karyotype differentiation, and also to developing a new variety.
Chromosomal Studies of the Hybrid between Female Rhodeus ocellatus ocellatus and Male Rhodeus atremius fangi in Bitterlings (Teleostei: Cypriniformes: Acheilognathinae)  [PDF]
Takayoshi Ueda, Yukie Ueda
Natural Resources (NR) , 2018, DOI: 10.4236/nr.2018.91002
Abstract:
The chromosome analysis of the masculinized hybrid between female Rhodeus ocellatus ocellatus and male R. atremius fangi in bitterlings (Acheilognathinae) was done. It was presumed that they had intermediate karyotype between the parents, and formed sperms with heteroploidy resulting from the incomplete pairing of homologous chromosomes in meiosis. Due to the abundance of species and the ease of artificial fertilization, the study of the factor of the hybrid sterility in bitterlings would lead to the clarification of the mechanism about species differentiation and karyotype differentiation, and also develop a new variety. And also, it would also be important to make the hybrid various natures clear in environmental preservation.
A Novel Source of Methylglyoxal and Glyoxal in Retina: Implications for Age-Related Macular Degeneration
Kee Dong Yoon, Kazunori Yamamoto, Keiko Ueda, Jilin Zhou, Janet R. Sparrow
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0041309
Abstract: Aging of retinal pigment epithelial (RPE) cells of the eye is marked by accumulations of bisretinoid fluorophores; two of the compounds within this lipofuscin mixture are A2E and all-trans-retinal dimer. These pigments are implicated in pathological mechanisms involved in some vision-threatening disorders including age-related macular degeneration (AMD). Studies have shown that bisretinoids are photosensitive compounds that undergo photooxidation and photodegradation when irradiated with short wavelength visible light. Utilizing ultra performance liquid chromatography (UPLC) with electrospray ionization mass spectrometry (ESI-MS) we demonstrate that photodegradation of A2E and all-trans-retinal dimer generates the dicarbonyls glyoxal (GO) and methylglyoxal (MG), that are known to modify proteins by advanced glycation endproduct (AGE) formation. By extracellular trapping with aminoguanidine, we established that these oxo-aldehydes are released from irradiated A2E-containing RPE cells. Enzyme-linked immunosorbant assays (ELISA) revealed that the substrate underlying A2E-containing RPE was AGE-modified after irradiation. This AGE deposition was suppressed by prior treatment of the cells with aminoguanidine. AGE-modification causes structural and functional impairment of proteins. In chronic diseases such as diabetes and atherosclerosis, MG and GO modify proteins by non-enzymatic glycation and oxidation reactions. AGE-modified proteins are also components of drusen, the sub-RPE deposits that confer increased risk of AMD onset. These results indicate that photodegraded RPE bisretinoid is likely to be a previously unknown source of MG and GO in the eye.
Mid and Far Infrared Properties of a Complete Sample of Local AGNs
Kohei Ichikawa,Yoshihiro Ueda,Yuichi Terashima,Shinki Oyabu,Poshak Gandhi,Keiko Matsuta,Takao Nakagawa
Physics , 2012, DOI: 10.1088/0004-637X/754/1/45
Abstract: We investigate the mid- (MIR) to far-infrared (FIR) properties of a nearly complete sample of local Active Galactic Nuclei (AGNs) detected in the Swift/BAT all sky hard X-ray (14-195 keV) survey, based on the cross correlation with the AKARI infrared survey catalogs complemented by those with IRAS and WISE. Out of 135 non-blazer AGNs in the Swift/BAT 9 month catalog, we obtain the MIR photometric data for 128 sources either in the 9, 12, 18, 22, and/or 25 um band. We find good correlation between their hard X-ray and MIR luminosities over 3 orders of magnitude (42< log lambda L_{lambda}(9, 18 um)< 45), which is tighter than that with the FIR luminosities at 90 um. This suggests that thermal emission from hot dusts irradiated by the AGN emission dominate the MIR fluxes. Both X-ray unabsorbed and absorbed AGNs follow the same correlation, implying isotropic infrared emission, as expected in clumpy dust tori rather than homogeneous ones. We find excess signals around 9 um in the averaged infrared spectral energy distribution from heavy obscured "new type" AGNs with small scattering fractions in the X-ray spectra. This could be attributed to the PAH emission feature, suggesting that their host galaxies have strong starburst activities.
NSC-induced D-neurons are decreased in striatum of schizophrenia: Possible cause of mesolimbic dopamine hyperactivity  [PDF]
Keiko Ikemoto
Stem Cell Discovery (SCD) , 2012, DOI: 10.4236/scd.2012.22009
Abstract: Neural stem cell (NSC) hypofunction is an etiological hypothesis of schizophrenia. Although dopamine (DA) dysfunction is also a widely accepted hypothesis, molecular background of mesolimbic DA hyperactivity has not yet been well known. Here, the author proposes “D-cell hypothesis”, accounting for molecular basis of mesolimbic DA hyperactivity of schizophrenia, by NSC hypofunction and decrease of putative NSC-induced D-cells. The “D-cell” is defined as “non-monoaminergic aromatic L-amino acid decarboxylase (AADC)-containing cell”. D-cells produce trace amines, and also take up amine precursors and convert them to amines by decarboxylation. The author reported “dopa-decarboxylating neurons specific to the human striatum”, that is, “D-neurons” in the human striatum, and decrease of striatal D-neurons in patients with schizophrenia. Trace amine-associated receptor, type 1 (TAAR1), a subtype of trace amine receptors, having a quite number of ligands such as tyramine, β-phenylethylamine (PEA) and methamphetamine, has modulating functions on monoamine neurons. It has been known that reduced binding of ligands to TAAR1 receptors on DA terminal of DA neurons of the midbrain ventral tegmental area (VTA) increased firing frequency of VTA DA neurons. In brains of schizophrenia, NSC hypofunction in the subventricular zone of lateral ventricle may cause decrease of D-neurons in the striatum and nucleus accumbens, and may result in decrease of trace amine signals. Decrease of trace amine signals to TAAR1 on VTA DA neurons may increase firing frequency of VTA DA neurons, and may finally cause mesolimbic DA hyperactivity. Increased stimulation to DA D2 receptors of NSCs might suppress NSC proliferation, and may induce additional mesolimbic DA hyperactivity as well as D-cell decrease. This novel theory, “D-cell hypothesis”, possibly explains mesolimbic DA hyperactivity in pathogenesis of schizophrenia.
D-Cell Hypothesis: Pathogenesis of Mesolimbic Dopamine Hyperactivity of Schizophrenia  [PDF]
Keiko Ikemoto
Journal of Behavioral and Brain Science (JBBS) , 2012, DOI: 10.4236/jbbs.2012.23048
Abstract: In the present article, the author proposes a new “D-cell hypothesis” for mesolimbic dopamine (DA) hyperactivity of schizophrenia, of which relevant molecular mechanism has not yet been known. The “D-cell” is defined as “the non-monoaminergic aromatic L-amino acid decarboxylase (AADC)-containing cell”. The D-cell contains AADC but not dopaminergic nor serotonergic. D-cells produce trace amines, and also take up amine precursors and convert them to amines by decarboxylation. The author reported “dopa-decarboxylating neurons specific to the human striatum”, that is, “D-neurons” in the human striatum, and preliminarily the number reduction of D-neurons in the striatum and nucleus accumbens of postmortem brains of patients with schizophrenia. Trace amine-associated receptor, type 1 (TAAR1), a subtype of trace amine receptors, having a large number of ligands, including tyramine, β-phenylethylamine (PEA), and methamphetamine, is a target receptor for the latest neuroleptic discovery. Recent studies have shown that the decreased stimulation of TAAR1 on cell membranes or nerve terminals of DA neurons in the midbrain ventral tegmental area (VTA) increased firing frequency of VTA DA neurons. In brains of schizophrenia, dysfunction of neural stem cells in the subventricular zone of lateral ventricle may cause reduction of the number of D-neurons in the striatum and nucleus accumbens, and may result in decrease of trace amine synthesis. The decrease of stimulation of TAAR1 on terminals of VTA DA neurons caused by trace amine reduction may increase firing frequency of VTA DA neurons, and may finally cause mesolimbic DA hyperactivity. This innovative theory, “D-cell hypothesis” might explain mesolimbic DA hyperactivity in pathogenesis of schizophrenia.
“D-cell hypothesis” of schizophrenia: possible theory for mesolimbic dopamine hyperactivity  [PDF]
Keiko Ikemot
World Journal of Neuroscience (WJNS) , 2012, DOI: 10.4236/wjns.2012.23021
Abstract: The author proposes a new “D-cell hypothesis” for mesolimbic dopamine (DA) hyperactivity of schizophrenia. The “D-cell” is defined as “non-monoaminergic aromatic L-amino acid decarboxylase (AADC)-containing cell”. D-cells produce trace amines, such as tyramine and β-phenylethylamine, and may also take up amine precursors and convert them to amines by decarboxylation. Trace amine-associated receptor, type 1 (TAAR1), a subtype of trace amine receptors, has a large number of ligands, including tyramine, β-phenylethylamine and methamphetamine, that influence on human mental states, and is now regarded to be a target receptor for novel neuroleptics. Recent studies revealed that the reduced stimulation of TAAR1 on DA neurons in the midbrain ventral tegmental area (VTA) increased firing frequency of VTA DA neurons. The author and her colleagues reported the decrease of D-neurons in the striatum and nucleus accumbens of postmortem brains of patients with schizophrenia. This may imply the decrease of trace amine synthesis, resulting the reduced stimulation of TAAR1 on terminals of midbrain VTA DA neurons, and may lead to mesolimbic DA hyperactivity in schizophrenia. The decrease of striatal D-neurons of postmortem brains of schizophrenia is supposed to be due to neural stem cell dysfunction in the subventricular zone of lateral ventricle. The decrease of striatal D-neurons and acts of TAAR1 signals on DA neurons-might explain mesolimbic DA hyperactivity of schizophrenia.
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