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47 results on '"Ishibashi, Tomoko"'

4. Intravenous immunoglobulin preparations attenuate lysolecithin-induced peripheral demyelination in mice and comprise anti-large myelin protein zero antibody

Author

SETOGUCHI, Yuki, primary, HAYASHI, Akiko, additional, KAWADA, Ayami, additional, IBUSUKI, Ayako, additional, YANAOKA, Daigo, additional, SAITO, Ryota, additional, ISHIBASHI, Tomoko, additional, TAKIMOTO, Hiroaki, additional, YAMAGUCHI, Yoshihide, additional, OHTAKI, Hirokazu, additional, and BABA, Hiroko, additional

Published
2023
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12. Alterations of NOS, arginase, and DDAH protein expression in rabbit cavernous tissue after administration of cigarette smoke extract

Author

Imamura, Masatoshi, Waseda, Yuma, Marinova, Galina Vasileva, Ishibashi, Tomoko, Obayashi, Satoshi, Sasaki, Akihito, Nagai, Akiko, and Azuma, Hiroshi

Subjects
Impotence -- Causes of, Immunohistochemistry -- Research, Rabbits -- Physiological aspects, Rabbits -- Diseases, Nitric oxide -- Influence, Nitric oxide -- Physiological aspects, Biological sciences
Abstract

Cigarette smoking is an independent risk factor for vasculogenic erectile dysfunction (ED). Nitric oxide (NO) has been demonstrated to be the principal mediator of cavernous smooth muscle relaxation and penile erection. Therefore, we examined whether or not enzyme activities and factors involved in the NO generation pathway are affected in rabbit corpus cavernosum after administration of nicotine- and tar-free cigarette smoke extract (CSE). CSE was prepared by bubbling a stream of cigarette smoke into phosphate-buffered saline. CSE was injected subcutaneously into adult male rabbits once a day for 5 wk. In the CSE group, significantly decreased cyclic GMP production as a marker of NO generation was associated with attenuated overall nitric oxide synthase (NOS) activity, enhanced arginase activity, accumulation of endogenous NOS inhibitors such as monomethylarginine (MMA) and asymmetric dimethylarginine (ADMA), and decreased dimethylarginine dimethylaminohydrolase (DDAH) activity as an metabolizing enzyme of endogenous NOS inhibitors. Neuronal NOS (nNOS) and DDAH I protein expression were decreased without altering endothelial NOS expression, while arginase I expression was upregulated. These results suggest that impaired NO production would result from blunted NOS activity, which is possibly brought about by the downregulation of nNOS protein, accumulation of endogenous NOS inhibitors, and enhanced arginase activity together with upregulation of arginase I protein in cavernous tissue. The impaired DDAH activity due to decreased expression of DDAH I protein would result in an accumulation of endogenous NOS inhibitors with CSE. These alterations may be relevant to induction of the erectile dysfunction following CSE. erectile dysfunction; nitric oxide generation pathway; anti-asymmetric dimethylarginine antibody; immunohistochemistry; Western blot

Published
2007

17. 957 – The Long-Term Consequences of the Donors After Living Donor Liver Transplantation; Predictors and Clinical Impact of Splenic Enlargement and Incomplete Liver Restoration

Author

Taura, Kojiro, primary, Yoshino, Kenji, additional, Ikeno, Yoshinobu, additional, Umeya, Yumi, additional, Ishibashi, Tomoko, additional, Kojitani, Yasuko, additional, Kimura, Yusuke, additional, Nam, Nguyen Hai, additional, Uemoto, Yusuke, additional, Fukumitsu, Ken, additional, Ito, Takashi, additional, Yagi, Shintaro, additional, Kamo, Naoko, additional, Hata, Koichiro, additional, Yamashiki, Noriyo, additional, Ueda, Yoshihide, additional, Kaido, Toshimi, additional, and Uemoto, Shinji, additional

Published
2019
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19. Lifestyle and T-helper 1 and 2 Related Cytokines in Healthy Volunteers

Author

MIURA, Yoshie, ISHIBASHI, Tomoko, TATSUKAWA, Tomohisa, MAEDA, Megumi, MURAKAMI, Shuko, NISHIMURA, Yasumitsu, KUMAGAI, Naoko, HAYASHI, Hiroaki, CHEN, Ying, HYODO, Fuminori, HATTA, Emiko, KOJIMA, Shinji, FUJII, Masafumi, MORIMOTO, Kanehisa, and OTSUKI, Takemi

Subjects
immunology, lifestyle, questionnaire, cytokine, Th1/2
Published
2008

20. Identification and Characterization of Tumor Initiating Cells in Various Mouse Mammary Tumor Models

Author

Ishibashi, Tomoko

Subjects
000 Generalities, Science
Abstract

Breast cancer is not a single disease as it can be classified into different subtypes according to cellular composition, morphology, proliferative index, genetic lesions and therapeutic responses. The molecular and cellular mechanisms underpinning tumor heterogeneity remain a central question in the cancer biology field. To explain the multitude of breast cancer phenotypes, it has been proposed that tumor-initiating cells (TICs) might originate from different cells within the mammary lineage. Further, different oncogenes might elicit distinct phenotypes in a given cell, adding to the complexity of the disease. Single oncogene amplification is observed in human breast tumors. For instance, the human epidermal growth factor receptor type-2 (HER2) proto-oncogene (also called ErbB2, or Neu) is amplified in about 20% of human breast cancers and associated with aggressive phenotypes and poor prognosis. Similarly, 16% of breast cancers have c-Myc gene amplification. Yet, it remains largely disputed which mammary cell type responds to a specific initiating oncogenic mutation. We decided to take a forward approach by testing two contrasting potent oncogenes, Neu (murine form of HER2) or c-Myc, that are frequently overexpressed in breast cancer patients for their capacity to transform different cells of the mammary lineage. A number of transgenic mouse mammary tumor models have been generated that mimic human breast cancers. Previous studies reported that TICs of Neu driven tumors are the luminal progenitor cells. These studies made use of a mouse model that constitutively overexpressed the Neu oncogene in mouse mammary glands under the MMTV promoter. In contrast, c-Myc overexpressing tumors show a heterogeneous mixed phenotype that is composed of both luminal and myoepithelial cells. Due to the presence of bi-lineage derived cells, we hypothesized that the TICs of c-Myc tumors are the bi-potent stem cells. To clarify the identity and characteristics of TICs, we employed tractable mouse models, Tet-On-Neu/MMTV- rtTA and Tet-On-Myc/MMTV-rtTA, in which we can induce the overexpression of an oncogene at any given time point by administration of doxycycline. The possibility to induce overexpression of an oncogene at adulthood (8-9 weeks after birth) closely recapitulates the timing of somatic mutations acquired by breast cancer patients. In order to demonstrate the direct contribution of distinct breast epithelial cellular lineages to Myc and Neu driven tumorigenesis, we took a FACS approach to separate bi-potent adult stem cells from lineage-committed progenitor cells and differentiated cells. We transplanted the purified cell populations, then induced oncogenes by administration of doxycycline and observed tumor formation in vivo. 9 These tumors obtained from the transplantation experiments were compared with the natural arising primary mammary tumors from Tet-On-Neu/MMTV-rtTA and Tet-On- Myc/MMTV-rtTA by their histological and molecular features. In parallel, we also monitored the clonal growth of these sorted cells in vitro after oncogene overexpression using organotypic 3D cell culture assays. Taken together and partially in contrast to our initial hypothesis, Neu induced tumors that are composed of luminal cells can originate not only from the luminal-committed progenitors but also from the bi-potent stem cells. Moreover, luminal committed progenitors were able to give rise to c- induced tumors that are composed of both luminal and myoepithelial lineages. We currently validate our findings by employing additional cell surface antibodies to closer define and sub-fractionate mammary cellular lineages and by an in vivo lineage tracing approach. Our results suggest that Neu and c-Myc TICs can arise from different cellular subtypes in the mammary gland. Notably, progenitor cells seem to be able to establish tumors that consist of basal and luminal cells. These results add to the growing notion that genetic predisposition directs cell fate towards distinct breast cancer phenotypes.

Published
2015
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42. A Case of Herpes Esophagitis Associated With Reflux Esophagitis

Author

Ishibashi, Tomoko, primary, Nakamura, Masaki, additional, Umetsu, Hitoshi, additional, Chiba, Kanenobu, additional, Hoshino, Kiyoshi, additional, Yoshikawa, Tomoko, additional, Nonaka, Kazuoki, additional, Kimura, Kanae, additional, Nakamura, Youichi, additional, Namiki, Masao, additional, Shimo, Masamune, additional, and Kato, Toshiaki, additional

Published
1993
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43. Evaluation of Endoscopic Resection of Gastric Tumors Following Local Injections of HSE (Hypertonic Saline‐Epinephrine Solution)

Author

NAKAMURA, Masaki, primary, ISHIBASHI, Tomoko, additional, TANIGUCHI, Hideto, additional, YAMAMOTO, Hitoshi, additional, NAKAJIMA, Yukihiro, additional, UMEZU, Hitoshi, additional, CHIBA, Kanenobu, additional, HOSHINO, Kiyoshi, additional, KIMURA, Kanae, additional, ISHII, Keiichi, additional, NAKAMURA, Youichi, additional, and UMETANI, Kaoru, additional

Published
1991
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44. Mice with Altered Myelin Proteolipid Protein Gene Expression Display Cognitive Deficits Accompanied by Abnormal Neuron--Glia Interactions and Decreased Conduction Velocities.

Author

Tanaka, Hisataka, Jianmei Ma, Tanaka, Kenji F., Takao, Keizo, Komada, Munekazu, Tanda, Koichi, Suzuki, Ayaka, Ishibashi, Tomoko, Baba, Hiroko, Isa, Tadashi, Shigemoto, Ryuichi, Ono, Katsuhiko, Miyakawa, Tsuyoshi, and Ikenaka, Kazuhiro

Subjects
LABORATORY mice, MYELIN genes, GENE expression, NEURONS, ASTROCYTES
Abstract

Conduction velocity (CV) of myelinated axons has been shown to be regulated by oligodendrocytes even after myelination has been completed. However, how myelinating oligodendrocytes regulate CV, and what the significance of this regulation is for normal brain function remain unknown. To address these questions, we analyzed a transgenic mouse line harboring extra copies of the myelin proteolipid protein 1 ( plp1) gene ( plp1tg/- mice) at 2 months of age. At this stage, the plp1tg/- mice have an unaffected myelin structure with a normally appearing ion channel distribution, but the CV in all axonal tracts tested in the CNS is greatly reduced. We also found decreased axonal diameters and slightly abnormal paranodal structures, both of which can be a cause for the reduced CV. Interestingly the plp1tg/- mice showed altered anxiety-like behaviors, reduced prepulse inhibitions, spatial learning deficits and working memory deficit, all of which are schizophrenia-related behaviors. Our results implicate that abnormalities in the neuron-glia interactions at the paranodal junctions can result in reduced CV in the CNS, which then induces behavioral abnormalities related to schizophrenia. [ABSTRACT FROM AUTHOR]

Published
2009
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45. Tetraspanin Protein CD9 Is a Novel Paranodal Component Regulating Paranodal Junctional Formation.

Author

Ishibashi, Tomoko, Lei Ding, Ikenaka, Kazuhiro, Inoue, Yoshiro, Miyado, Kenji, Mekada, Eisuke, and Baba, Hiroko

Subjects
*ION channels, *ION-permeable membranes, *MYELINATION, *NERVES, *MYELIN proteins
Abstract

The axoglial paranodal junction is essential for the proper localization of ion channels around the node of Ranvier. The integrity of this junction is important for nerve conduction. Although recent studies have made significant progress in understanding the molecular composition of the paranodal junction, it is not known how these membrane components are distributed to the appropriate sites and interact with each other. Here we show that CD9, a member of the tetraspanin family, is present at the paranode. CD9 is concentrated in the paranode as myelination proceeds, but CD9 clusters become diffuse, associated with disruption of the paranode, in cerebroside sulfotransferase-deficient mice. Immunohistochemical and Western blot analysis showed that CD9 is distributed predominantly in the PNS. Ablation of CD9 in mutant mice disrupts junctional attachment at the paranode and alters the paranodal components contactinassociated protein (also known as Paranodin) and neurofascin 155, although the frequency of such abnormalities varies among individuals and individual axons even in the same mouse. Electron micrographs demonstrated that compact myelin sheaths were also affected in the PNS. Therefore, CD9 is a myelin protein important for the formation of paranodal junctions. CD9 also plays a role in the formation of compact myelin in the PNS. [ABSTRACT FROM AUTHOR]

Published
2004
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