Search

Your search keyword '"Ezaki, Taichi"' showing total 242 results
Start Over Author "Ezaki, Taichi"
242 results on '"Ezaki, Taichi"'

69. A Novel Chemical Compound, NK026680, Targets Dendritic Cells to Prolong Recipient Survival After Rat Liver Grafting

Author

Hara, Yoshiaki, primary, Funeshima-Fuji, Naoko, additional, Fujino, Masayuki, additional, Tokunaka, Kazuhiro, additional, Abe, Fuminori, additional, Sato, Yoshinobu, additional, Hatakeyama, Katsuyoshi, additional, Takahara, Shiro, additional, Ezaki, Taichi, additional, Kimura, Hiromitsu, additional, and Li, Xiao-Kang, additional

Published
2007
Full Text
View/download PDF

71. Defective B1 Cell Homing to the Peritoneal Cavity and Preferential Recruitment of B1 Cells in the Target Organs in a Murine Model for Systemic Lupus Erythematosus

Author

Ito, Toshihiro, primary, Ishikawa, Sho, additional, Sato, Taku, additional, Akadegawa, Kenji, additional, Yurino, Hideaki, additional, Kitabatake, Masahiro, additional, Hontsu, Shigeto, additional, Ezaki, Taichi, additional, Kimura, Hiroshi, additional, and Matsushima, Kouji, additional

Published
2004
Full Text
View/download PDF

78. In Vivo Migration of Rat Dendritic Cells.

Author

Walker, John M., Robinson, Stephen P., Stagg, Andrew J., Knight, Stella C., Matsuno, Kenjiro, and Ezaki, Taichi

Abstract

Dendritic cells (DCs) comprise a dynamic cellular system with a continuous traffic throughout the body. DCs connect nonlymphoid and lymphoid tissues via the lymph and blood, and transport antigenic information from most parts of the body to the immune system (1). To understand the migratory behavior of DCs in vivo is very important, because in different immunological situations, this behavior could change easily and, in turn, greatly affect immune responses (2). Factors that determine the behavior of DCs, such as adhesion molecules, could potentially be the targets for manipulating and regulating immune responses. The study of DC migration, therefore, should provide useful information for understanding the role of DCs not only in local but also in systemic host-defense mechanisms (3). The aim of this chapter is to introduce several useful methods that help to examine DC migration in vivo. [ABSTRACT FROM AUTHOR]

Published
2001
Full Text
View/download PDF

79. A T cell activation antigen, Ly6C, induced on CD4+ Th1 cells mediates an inhibitory signal for secretion of IL-2 and proliferation in peripheral immune responses

Author

Yamanouchi, Sachiko, primary, Kuwahara, Kazuhiko, additional, Sakata, Atsuko, additional, Ezaki, Taichi, additional, Matsuoka, Shuji, additional, Miyazaki, Jun-ichi, additional, Hirose, Sachiko, additional, Tamura, Toshiki, additional, Nariuchi, Hideo, additional, and Sakaguchi, Nobuo, additional

Published
1998
Full Text
View/download PDF

86. Fine structural study of the innervation of muscle spindles in the internal oblique muscle of the abdominal wall in the adult mouse.

Author

Desaki, Junzo, Ezaki, Taichi, and Nishida, Naoya

Subjects
*MUSCLE physiology, *INNERVATION, *ABDOMINAL wall, *ELECTRON microscopy, *LABORATORY mice
Abstract

We examined by electron microscopy the innervation of muscle spindles in the internal oblique muscle of the mouse abdominal wall. In the equatorial region, in addition to the sensory innervation on individual intrafusal muscle fibers, sensory cross terminals were often observed between nuclear chain fibers. In the area from the juxtaequatorial region to the polar region, nuclear bag fibers were supplied by trail and plate-type motor endings, while nuclear chain fibers were innervated by sensory endings, being probably secondary sensory endings. From these findings, it is clear that the innervation patterns differ between two types of intrafusal muscle fibers. [ABSTRACT FROM PUBLISHER]

Published
2010
Full Text
View/download PDF

89. Discontinuous capillary segments in the extensor digitorum longus muscle of aged BUF/Mna rats.

Author

Desaki, Junzo and Ezaki, Taichi

Abstract

We examined the structural changes of capillaries in the extensor digitorum longus muscle of aged (25 months) male BUF/Mna rats, which caused severe muscle weakness of hind legs during aging. The aged muscle mostly consisted of bundles of muscle fibres 15–35 µm in diameter (type 1). In some small areas, however, muscle bundles contained small muscle fibres mainly 15–25 µm in diameter (type 2), possibly indicating that these small fibres are in the course of regeneration after necrosis. Examination of serial ultrathin sections revealed some remarkable changes of capillaries in the type 2 muscle bundle. In some capillaries, the vascular lumen became discontinuous by several close contacts of opposed endothelial cells in their course, forming plural closed vascular segments. Moreover, a solitary endothelial cell was often observed within a scaffold of basal lamina, which remained after destruction of endothelial cells. The segmentation of capillaries and the occurrence of the scaffolds of basal laminae are considered to indicate the degenerative process of capillaries. In some instances, on the other hand, endothelial cells closely apposed each other with no vascular lumen for distances of up to 100 µm, and some capillaries had a narrow vascular lumen (1–3 µm diameter) for a long distance (∼300 µm), probably indicating that these structures are in the course of regenerating capillaries to remodel the capillary networks around the muscle fibres. Pericytic processes circularly arranged outside the endothelium at the slit‐like and narrow vascular lumen, like hoops, possibly preventing the rupture of the newly‐formed vascular lumen from the increased blood flow and/or blood pressure. In addition, the occasional occurrence of capillaries with fenestrations may participate to increase the supply of nutrients and oxygen to the regenerating muscle fibres. The present findings suggest that the capillary networks in the extensor digitorum longus muscle of aged BUF/Mna rats are remodelled following the regeneration of muscle fibres after necrosis, and that on occasion, neighbouring endothelial cells may closely contact with each other both in the degenerative and regenerative processes of capillaries. [ABSTRACT FROM PUBLISHER]

Published
2002
Full Text
View/download PDF

95. Reduced T cell expansion by a superantigen as a result of impaired B cell development in mice deficient for the p85α regulatory subunit of PI3K

Author

Arimura, Yutaka, Ezaki, Taichi, Koyanagi, Madoka, Uchiyama, Takehiko, Koyasu, Shigeo, and Yagi, Junji

Abstract

PI3K p85α subunit alters the superantigen presentation capacity of B cells and indirectly modulates the magnitude of the T cell response. PI3K plays crucial roles in the immune system. Mice deficient for p85α, a major regulatory subunit of class IA PI3K, show various defects and alterations in B cells, mast cells, macrophages, and DCs, and peripheral T cells are reportedly normal, at least in vitro. In normal mice, long‐term exposure to a SAg, SEA, in vivo induced a high level of the protracted expansion of SEA‐reactive Vβ3+CD4+T cells, whereas the same treatment induced T cell expansion in p85α‐deficient mice but to a much lesser extent than in normal mice. However, mixed bone marrow chimera mice, which have normal and p85α‐deficient T and B cells, demonstrated equal responses of both T cells following stimulation with a SEA pump. In reciprocal cotransfer experiments of T and B cells from normal and p85α‐deficient mice into Rag2‐deficient mice, followed by SEA stimulation, p85α‐deficient T cells revealed much higher proliferative capacity in the presence of normal B cells than did normal T cells with p85α‐deficient B cells. Histologically, a marked B cell reduction was observed in the follicles and MZ of the spleen, and DCs accumulated in the MZ. In addition, p85α‐deficient B cells had a low level of MHC class II expression. Collectively, these data suggested that the PI3K p85α subunit alters the SAg presentation capacity of B cells and indirectly modulates the magnitude of the T cell response, which may affect the protection against SEA‐containing bacteria.

Published
2010
Full Text
View/download PDF

98. Remodelling of capillary networks around muscle fibres in the extensor digitorum longus muscle of the normal aged rat

Author

Desaki, Junzo, Oki, Sadaaki, and Ezaki, Taichi

Abstract

Structural changes of capillaries around muscle fibres following their degeneration and regeneration were further examined in the extensor digitorum longus muscle of the 24‐month‐old normal rat. Bundles of muscle fibres were divided into three types: muscle bundles consisting of large muscle fibres exclusively more than 35 µm in diameter (type 1), various‐sized muscle fibres ranging from 10 to 60 µm in diameter (type 2) and only small muscle fibres 20–40 µm in diameter (type 3). The mean number of capillaries around a muscle fibre was extremely high in the type 3 muscle bundle (4.83) and much lower in the type 2 muscle bundle (2.72) compared with that in the type 1 muscle bundle (3.48). Capillaries in the type 1 muscle bundle were round or oval in shape and were of the continuous type. In the type 2 muscle bundle, capillaries around large degenerating muscle fibres showed an irregularly compressed shape and the scaffolds of basal laminae were often found around them, being a result of the destruction of capillaries. On the other hand, small‐sized capillaries less than 5 µm in diameter, being possibly regenerating capillaries, were found around small (probably regenerating) muscle fibres and often had a small number (less than 10) of fenestrae. Capillaries in the type 3 muscle bundle, similar in shape and size to those in the type 1, frequently branched or joined, but some of them were partially destroyed. These findings suggest that capillaries degenerate and regenerate to remodel capillary networks around the muscle fibres following their degeneration and regeneration, and that to effectively supply oxygen and nutrients to regenerating muscle fibres, capillaries temporarily form fenestrae and then the capillary networks become dense by sprouts from the existing capillaries, but excess capillaries may be gradually destroyed following maturation of the muscle fibres.

Published
2002
Full Text
View/download PDF

99. Aged neuromuscular junctions in the extensor digitorum longus muscle of the rat as revealed by scanning electron microscopy

Author

Oki, Sadaaki, Desaki, Junzo, Ezaki, Taichi, and Matsuda, yoshiro

Abstract

We examined the overall morphology of subneural apparatuses (SNAs) at neuromuscular junctions by scanning electron microscopy in the extensor digitorum longus muscle of aged (18 months) rats. Most of aged SNAs were mainly characterized by a large number (more than 20) of cup-like depressions (2–5 urn in diameter) with numerous slit-like junctional folds about 0.1 urn wide and 5 urn at maximum length, while some SNAs consisted of a small number (fewer than 10) of depressions or poorly-developed gutters containing pit-like and/or slit-like junctional folds. Additionally, numerous slits were often found outside the depressions, possibly indicating the preexisting junctional folds persisted for a long time after the gutter-into-cup transformation of the SNAs. These structural changes of SNAs during ageing are discussed briefly.

Published
1999
Full Text
View/download PDF

100. Morphological and functional characterization of non-alcoholic fatty liver disease induced by a methionine-choline-deficient diet in C57BL/6 mice.

Author

Itagaki H, Shimizu K, Morikawa S, Ogawa K, and Ezaki T

Subjects
Alanine Transaminase blood, Animals, Antigens, CD metabolism, Antigens, Differentiation, Myelomonocytic metabolism, Aspartate Aminotransferases blood, Biomarkers blood, Cell Proliferation, Chemokine CCL2 genetics, Chemokine CCL2 metabolism, Choline Deficiency blood, Disease Models, Animal, Fatty Liver blood, Fatty Liver pathology, Gene Expression Regulation, Kupffer Cells metabolism, Kupffer Cells ultrastructure, Liver metabolism, Liver Cirrhosis etiology, Liver Cirrhosis pathology, Male, Matrix Metalloproteinase 13 genetics, Matrix Metalloproteinase 13 metabolism, Matrix Metalloproteinase 9 genetics, Matrix Metalloproteinase 9 metabolism, Mice, Mice, Inbred C57BL, Non-alcoholic Fatty Liver Disease, Proliferating Cell Nuclear Antigen metabolism, RNA, Messenger metabolism, Time Factors, Choline Deficiency complications, Fatty Liver etiology, Liver ultrastructure, Methionine deficiency
Abstract

Background: Non-alcoholic fatty liver disease (NAFLD), including non-alcoholic steatohepatitis (NASH), appears to be increasingly common worldwide. Its histopathology and the effects of nutrition on liver function have not been fully determined., Aim: To elucidate the cellular mechanisms of NAFLD induced by a methionine-choline-deficient (MCD) diet in mice. Particular focus was placed on the role of phagocytic cells., Methods: Male C57BL/6 mice were fed an MCD diet for 30 weeks. A recovery model was also established wherein a normal control diet was provided for 2 weeks after a period of 8, 16, or 30 weeks., Results: Mice fed the MCD diet for ≥ 2 weeks exhibited severe steatohepatitis with elevated serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. Steatohepatitis was accompanied by the infiltration of CD68-positive macrophages (Kupffer cells). The severity of steatohepatitis increased in the first 16 weeks but was seen to lessen by week 30. Fibrosis began to develop at 10 weeks and continued thereafter. Steatohepatitis and elevated serum hepatic enzyme concentrations returned to normal levels after switching the diet back to the control within the first 16 weeks, but fibrosis and CD68-positive macrophages remained., Conclusions: The histopathological changes and irreversible fibrosis seen in this model were caused by prolonged feeding of an MCD diet. These results were accompanied by changes in the activity of CD68-positive cells with temporary elevation of CCL-2, MMP-13, and MMP-9 levels, all of which may trigger early steatohepatitis and late fibrosis through phagocytosis-associated MMP induction.

Published
2013

Catalog

Books, media, physical & digital resources
See catalog results