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600 results on '"Kirino, Y."'

52. Involvement of brain oxidation in the cognitive impairment in a triple transgenic mouse model of Alzheimer's disease: Noninvasive measurement of the brain redox state by magnetic resonance imaging

Author

Ishihara, Y., primary, Itoh, K., additional, Mitsuda, Y., additional, Shimada, T., additional, Kubota, T., additional, Kato, C., additional, Song, S. Y., additional, Kobayashi, Y., additional, Mori-Yasumoto, K., additional, Sekita, S., additional, Kirino, Y., additional, Yamazaki, T., additional, and Shimamoto, N., additional

Published
2013
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70. Role of Src in hypersensitization to phosphodiesterase inhibitors in beta2-adrenoceptor-desensitized eosinophils

Author

Fujii Y, Kirino Y, Mitsunobu Mio, and Kamei C

Subjects
Male, medicine.medical_specialty, Eosinophil Peroxidase, Time Factors, Phosphodiesterase Inhibitors, medicine.drug_class, medicine.medical_treatment, Guinea Pigs, Genistein, In Vitro Techniques, Biology, SRC Family Tyrosine Kinase, Cell Degranulation, Tyrosine-kinase inhibitor, chemistry.chemical_compound, Internal medicine, medicine, Animals, heterocyclic compounds, Calcimycin, Rolipram, Fenoterol, Desensitization (medicine), Ionophores, Phosphodiesterase, Adrenergic beta-Agonists, respiratory system, Eosinophils, Pyrimidines, src-Family Kinases, Endocrinology, Peroxidases, chemistry, Enzyme inhibitor, biology.protein, Receptors, Adrenergic, beta-2, sense organs, medicine.drug, Proto-oncogene tyrosine-protein kinase Src
Abstract

When guinea pig eosinophils were incubated with fenoterol, a beta2-agonist, for 120 min, not only desensitization of beta2-adrenoceptors but also hyperresponsiveness to phosphodiesterase (PDE) inhibitors, such as theophylline and rolipram, was observed. The fenoterol-induced beta2-adrenoceptor desensitization was not affected by pretreatment with either genistein, a broad-spectrum tyrosine kinase inhibitor, or PP2, a specific Src family tyrosine kinase inhibitor. On the other hand, both genistein and PP2 abolished the hyperresponsiveness to PDE inhibitors in beta2-adrenoceptor-desensitized eosinophils. These findings suggested that Src family tyrosine kinases play important roles in the hypersensitization of PDE to PDE inhibitors in beta2-adrenoceptor-desensitized eosinophils.

Published
2003
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87. 389 Phosphorylation of APLP2 in cell cycle-dependent manner

Author

Andoo, K., primary, Satoh, Y., additional, Isohara, T., additional, Oishi, M., additional, Iijima, K., additional, Lim, G.S., additional, Wasco, W., additional, Tanzi, R.E., additional, Naim, A.C., additional, Kirino, Y., additional, Greengard, P., additional, Gandyl, S.E., additional, and Suzuki, T., additional

Published
1996
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90. Comparing patient dissatisfaction and rational judgment in intentional medication non-adherence versus unintentional non-adherence.

Author

Iihara, N., Nishio, T., Okura, M., Anzai, H., Kagawa, M., Houchi, H., and Kirino, Y.

Subjects
CONFIDENCE intervals, DRUGS, EPIDEMIOLOGY, HEALTH behavior, PATIENT-professional relations, PATIENT compliance, PATIENT satisfaction, QUESTIONNAIRES, RESEARCH funding, U-statistics, DATA analysis, CROSS-sectional method, DATA analysis software, DESCRIPTIVE statistics
Abstract

What is known and objective Patients' poor adherence to medications is reported to be related to the individual patients' beliefs and cognitions and their trust of the medical staff. However, the causes of the two forms of non-adherence, intentional and unintentional behaviours, have yet to be clarified. This study compared psychological latent factors associated with intentional and unintentional non-adherence to chronic medication regimens, focusing on the potential effects of (i) patients' dissatisfaction with treatment and their relationships with the medical staff and (ii) patients' subliminal rational thinking processes, which weighed the positive values such as their expectations of benefits from treatment against negative values such as their dissatisfaction. Methods Two cross-sectional surveys were undertaken of patients given medications for chronic diseases, using a questionnaire developed and validated in this study. One survey was undertaken in three hospitals and the other survey, online throughout Japan. We scored the individual latent factors using the questionnaire and calculated the differential score between two negatively correlated latent factors to quantify patients' subliminal rational thinking process. We compared the adjusted odds ratio ( OR) of latent factors between intentional and unintentional non-adherence to medication in both surveys. Results and discussion Of the eligible subjects, 149 hospitalized patients and 524 survey participants completed the questionnaire. Intentional non-adherence was associated with patient dissatisfaction with treatment including interpersonal relationships with medical staff in both hospitalized patients and online survey participants (95% confidence interval of adjusted OR for Dissatisfaction, 1·20-16·26 in the hospital-based survey and 1·33-3·45 in the online survey). In both surveys, intentional non-adherence was significantly associated with the differential score between two negatively correlated latent factors, Willingness and Dissatisfaction ( P = 0·02 in the hospital-based survey and P < 0·001 in the online survey). However, these associations were not evident in unintentionally non-adherent patients. What is new and conclusions Patients' dissatisfaction and their resulting rational judgments are unique, consistent determinants of intentional non-adherence to medications, but not of unintentional non-adherence. [ABSTRACT FROM AUTHOR]

Published
2014
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91. Erratum

Author

Shinozaki, K., primary, Anzai, K., additional, Kirino, Y., additional, Lee, S., additional, and Aoyagi, H., additional

Published
1994
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99. Variable penetrance of a familial progressive necrotising encephalopathy due to a novel tRNAIle homoplasmic mutation in the mitochondrial genome.

Author

Limongelli, A., Schaefer, J., Jackson, S., Invernizzi, F., Kirino, Y., Suzuki, T., Reichmann, H., and Zeviani, M.

Subjects
FAMILIAL diseases, GENETIC disorders, TRANSFER RNA, GENETIC mutation, MITOCHONDRIA, GENOMES
Abstract

Introduction: We present a family comprising a clinically normal mother and two daughters, each with severe encephalopathy with onset in late childhood. A third daughter had died previously of an earlier onset but neuropathologically similar disease. Methods: Sequence analysis of the entire mtDNA was carried out in muscle, fibroblasts, and lymphocytes of the affected daughters and unaffected mother. Biochemical analysis of individual respiratory chain enzymes was performed on the same tissues, and on several transmitochondrial cybrid clones containing the nucleus of a 143B.206 osteosarcoma cell line and the mutant mtDNA. Results: Genetic analyses revealed in both daughters and mother the presence of a novel mutation in the tRNAIle gene of mtDNA, which was homoplasmic in fibroblasts, lymphocytes, and skeletal muscle of the two patients. It was also homoplasmic in fibroblast and skeletal muscle samples of the mother, and approximately 97% heteroplasmic in her lymphocytes. Combined defects of complexes I and IV of the mitochondrial respiratory chain were found not only in fibroblasts of the two probands, but surprisingly also in those of their clinically unaffected mother. The respiratory chain defect segregated in transmitochondrial cybrids containing the nucleus of a 143B.206 osteasarcoma cell line and the mutant mtDNA, indicating that the latter was responsible for the biochemical phenotype. Discussion: Our results support the concept that homoplasmic mutations in tRNA genes can be responsible for mitochondrial disorders characterised by extremely variable penetrance. Albeit still unexplained, this phenomenon has important consequences in the nosological characterisation, clinical management, and genetic counselling of mitochondrial disorders. [ABSTRACT FROM AUTHOR]

Published
2004
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100. Phospholipase Cbeta4 and protein kinase Calpha and/or protein kinase CbetaI are involved in the induction of long term depression in cerebellar Purkinje cells.

Author

Hirono, M, Sugiyama, T, Kishimoto, Y, Sakai, I, Miyazawa, T, Kishio, M, Inoue, H, Nakao, K, Ikeda, M, Kawahara, S, Kirino, Y, Katsuki, M, Horie, H, Ishikawa, Y, and Yoshioka, T

Abstract

Activation of the type-1 metabotropic glutamate receptor (mGluR1) signaling pathway in the cerebellum involves activation of phospholipase C (PLC) and protein kinase C (PKC) for the induction of cerebellar long term depression (LTD). The PLC and PKC isoforms that are involved in LTD remain unclear, however. One previous study found no change in LTD in PKCgamma-deficient mice, thus, in the present study, we examined cerebellar LTD in PLCbeta4-deficient mice. Immunohistochemical and Western blot analyses of cerebellum from wild-type mice revealed that PLCbeta1 was expressed weakly and uniformly, PLCbeta2 was not detected, PLCbeta3 was expressed predominantly in caudal cerebellum (lobes 7-10), and PLCbeta4 was expressed uniformly throughout. In PLCbeta4-deficient mice, expression of total PLCbeta, the mGluR1-mediated Ca(2+) response, and LTD induction were greatly reduced in rostral cerebellum (lobes 1-6). Furthermore, we used immunohistochemistry to localize PKCalpha, -betaI, -betaII, and -gamma in mouse cerebellar Purkinje cells during LTD induction. Both PKCalpha and PKCbetaI were found to be translocated to the plasmamembrane under these conditions. Taken together, these results suggest that mGluR1-mediated activation of PLCbeta4 in rostral cerebellar Purkinje cells induced LTD via PKCalpha and/or PKCbetaI.

Published
2001
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