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42 results on '"Sun, Xue-Zhi"'

1. Animal Models of Xeroderma Pigmentosum

Author

Sun, Xue-Zhi, Zhang, Rui, Cui, Chun, Harada, Yoshi-Nobu, Hisano, Setsuji, Gu, Yeunhwa, Fukui, Yoshihiro, Yonehara, Hidenori, Back, Nathan, editor, Cohen, Irun R., editor, Lajtha, Abel, editor, Lambris, John D., editor, Paoletti, Rodolfo, editor, Ahmad, Shamim I., editor, and Hanaoka, Fumio, editor

Published
2009
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8. Expression of neural cell adhesion molecule L1 in the brain of rats exposed to X-irradiation in utero

Author

Sun, Xue-Zhi, Zhang, Rui, Cui, Chun, Takahashi, Sentaro, Kubota, Yoshihisa, Sawada, Kazuhiko, and Fukui, Yoshihiro

Subjects
irradiation, neocortex, migration, cell adhesion molecular
Abstract

To gain insight to the cellular and molecular mechanisms involved abnormal neuronal migration induced by irradiation, we investigated expression of neuronal cell adhesion molecule L 1 and neuronal migration in the brains through comparison between rats prenatally exposed to X-ray and controls. To observe the pattern of neuronal migration, bromodeoxyuridine (BrdU) was chosen as a marker to label migrating cells. The results showed some of the labeled cells remained in the lower of the cortical plate in the irradiated rats, suggesting that neuronal migration was disrupted by X-ray. To study change of expressing neural cell molecule L1, rat brains were analyzed by SDS-PAGE after isolation of L1 by immunoaffinity chromatography. In the all brain membrane fraction, immunoaffinity purified L1 had bands at 200, 180, 140 and 80 kDa. However, the bands in the irradiated group were very weak when compared with the control. Taking these results into account, abnormal neuronal migration and reduction of expression L1 found in their radiated brain indicated that migration of neural cells may be largely dependent on radial glial fiber as well as neural cell molecules like L1. A decrease in L1 expressionmay be one of reasons of abnormal neuronal migration.

Published
2003

9. Distribution of calbindin-D28K immunoreactive neurons in rat primary motor cortex

Author

Sun, Xue-Zhi, Takahashi, Sentaro, Cui, Chun, Inoue, Minoru, and Fukui, Yoshihiro

Subjects
immunocytochemistry, primary motor cortex, nervous system, calbindin-D28K, GABAergic neuron, calcium-binding protein
Abstract

Distribution of calbindin-D28K immunoreactive cells in the primary motor area of the adult rat neocortex was studied in the present experiment. In the primary motor cortex, calbindin-D28K immunoreactivity was found in two populations of cortical neurons. One was composed of neurons heavily labeled with anti-calbindin antibody, which were present in two bands corresponding to cortical layers II-III, and V. The morphological types of these cells were varied they had oval, fusiform or mutiangular somata. The proximal dendrites of the heavily stained cells showed that these cells were non-pyramidal neurons, and they were either bitufted or multipolar cells. The other was a weakly stained population, mainly concentrated in layers II and III, that also contained pyramidal neurons. In addition, one outstanding feature of the neuropil staining deep to layer II was the labeling of the long, vertically oriented bundles of immunoreactive processes. Such a distinct pattern of calbindin-D28K immunoreactive neurons in the primary motor cortex suggests a relatively high density of calcium channels exists in the superficial layers of the rat primary motor cortex.

Published
2002

10. Animal Models of Xeroderma Pigmentosum

Author

Sun, Xue-Zhi, primary, Zhang, Rui, additional, Cui, Chun, additional, Harada, Yoshi-Nobu, additional, Hisano, Setsuji, additional, Gu, Yeunhwa, additional, Fukui, Yoshihiro, additional, and Yonehara, Hidenori, additional

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11. Spatial learning and expression of neural cell adhesion molecule L1 in rats X-irradiated prenatally

Author

Zhang, Rui, Sun, Xue-Zhi, Cui, Chun, Sakata-Haga, Hiromi, Sawada, Kazuhiko, Ye, Changli, Fukui, Yoshihiro, Zhang, Rui, Sun, Xue-Zhi, Cui, Chun, Sakata-Haga, Hiromi, Sawada, Kazuhiko, Ye, Changli, and Fukui, Yoshihiro

Abstract

The present study was designed to present evidence to clarify the relationships between learning ability, neuronal cell adhesion molecule L1 expression and hippocampal structural changes in the rat model received X-irradiation at an embryonic stage (E15). Water maze task indicated that all of the irradiated rats failed to learn the task in the whole training procedure. Their latency to the platform and swimming distance were significant differences from those sham-treated controls. Histological studies showed that the hippocampal ectopias induced by X-rays in the CA1 were involved in the spatial learning impairment, in which they hampered normal processes in learning development and transmission of information. Number, size and positions of the ectopias in the dorsal parts of the hippocampus were confirmed to be related to degrees of spatial learning impairment. On the other hand, L1 expression in the hippocampus was examined with Western blot analysis. The results indicated a lower content of L1 in the irradiated rats. A decrease in L1 might be one of reasons to cause disorganization of the septohippocampal pathways. These findings suggest some mechanisms of spatial learning impairment can be attributed to the formation of the hippocampal ectopias and redaction of L1 following prenatal exposure to X-irradiation.

Published
2007

12. Experimental model for irradiating a restricted region of the rat brain using heavy-ion beams

Author

Sun, Xue-Zhi, Takahashi, Sentaro, Kubota, Yoshihisa, Zhang, Rui, Cui, Chun, Nojima, Kumie, Fukui, Yoshihiro, Sun, Xue-Zhi, Takahashi, Sentaro, Kubota, Yoshihisa, Zhang, Rui, Cui, Chun, Nojima, Kumie, and Fukui, Yoshihiro

Abstract

Heavy-ion beams have the feature to administer a large radiation dose in the vicinity of the endpoint in the beam range, its irradiation system and biophysical characteristics are different from ordinary irradiation instruments like X-rays or gamma-rays. In order to get clarify characteristic effects of heavy-ion beams on the brain, we have developed an experimental system for irradiating a restricted region of the rat brain using heavy-ion beams. The left cerebral hemispheres of the adult rat brain were irradiated at dose of 50Gy charged carbon particles (290MeV/nucleon 5mmspread-out Bragg peak). After irradiation, the characteristics of the heavy-ion beams and the animal model were studied. Histological examination and measurement showed that extensive necrosis was observed between 2.5mmand7.5mmdepth from the surface of the rat head, suggesting a relatively high dose and uniform dose was delivered among designed depths and the spread-out bragg peak used here successfully and satisfactorily retained its high-dose localization in the defined region. We believe that our experimental model for irradiating a restricted region of the rat brain using heavy-ion beams is a good model for analyzing regional radiation susceptibility of the brain.

Published
2004

15. Normal and abnormal neuronal migration in the developing cerebral cortex

Author

Sun, Xue-Zhi, Takahashi, Sentaro, Cui, Chun, Zhang, Rui, Sakata-Haga, Hiromi, Sawada, Kazuhiko, Fukui, Yoshihiro, Sun, Xue-Zhi, Takahashi, Sentaro, Cui, Chun, Zhang, Rui, Sakata-Haga, Hiromi, Sawada, Kazuhiko, and Fukui, Yoshihiro

Abstract

Neuronal migration is the critical cellular process which initiates histogenesis of cerebral cortex. Migration involves a series of complex cell interactions and transformation. After completing their final mitosis, neurons migrate from the ventricular zone into the cortical plate, and then establish neuronal lamina and settle onto the outermost layer, forming an “inside-out” gradient of maturation. This process is guided by radial glial fibers, requires proper receptors, ligands, other unknown extracellular factors, and local signaling to stop neuronal migration. This process is also highly sensitive to various physical, chemical and biological agents as well as to genetic mutations. Any disturbance of the normal process may result in neuronal migration disorder. Such neuronal migration disorder is believed as major cause of both gross brain malformation and more special cerebral structural and functional abnormalities in experimental animals and in humans. An increasing number of instructive studies on experimental models and several genetic model systems of neuronal migration disorder have established the foundation of cortex formation and provided deeper insights into the genetic and molecular mechanisms underlying normal and abnormal neuronal migration.

Published
2002

37. Abnormal expression of tyrosine hydroxylase not accompanied by phosphorylation at serine 40 in cerebellar Purkinje cells of ataxic mutant mice, rolling mouse Nagoya anddilute-lethal.

Author

Sawada, Kazuhiko, Ando, Masahiro, Sakata-Haga, Hiromi, Sun, Xue-Zhi, Jeong, Young-Gil, Hisano, Setsuji, Takeda, Noriaki, and Fukui, Yoshihiro

Subjects
TYROSINE, PHOSPHORYLATION, IMMUNOHISTOCHEMISTRY techniques, PURKINJE cells, LABORATORY mice, CHEMICAL reactions
Abstract

This study examined immunohistochemically the expression of an enzymatically active form of tyrosine hydroxylase (TH), phosphorylated TH at Ser40 (phospho-TH), in the cerebellum of ataxic mutant mice, rolling mouse Nagoya (RMN) anddilute-lethal(DL). TH immunostaining appeared in some Purkinje cells in RMN and DL, but in a few of the Purkinje cells of littermate controls for both mutants. In all groups of mice, there were no phospho-TH immunoreactive Purkinje cells in the cerebellum, although the subsets of TH immunoreactive Purkinje cells were found in the adjacent sections. The results suggest that TH expression in the Purkinje cells of ataxic mutants abnormally increases without activation of this enzyme by phosphorylation. This may mean that TH in Purkinje cells is not related to catecholamine synthesis. [ABSTRACT FROM AUTHOR]

Published
2004
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39. An Immunohistochemical Study of Radial Glial Cells in the Mouse Brain Prenatally Exposed to {gamma}-irradiation

Author

Sun, Xue-Zhi, Inouye, Minoru, Fukui, Yoshihiro, Hisano, Setsuji, Sawada, Kazuhiko, Muramatsu, Hisako, and Muramatsu, Takashi

Abstract

The features of a glial cell population in the developing brain of mice prenatally exposed to 60Co γ-irradiation at the most radiosensitive stage were studied with immunohistochcmistry for anti-midkine (MK), anti-vimentin (Vim), and anti-GFAP antibodies. Anti-MK- and anti-Vim-positive radial glial fibers distributed in a similar radial fashion; these fibers were observed primarily in the embryonic period and disappeared after birth. Anti-MK- and anti-Vim-staincd radial fibers ran perpendicular to the pial surface in controls, whereas such fibers were disorganized 6 hours (h) after irradiation. This finding provided new evidence that the migratory pathways of young neurons were interrupted beginning a few hours after irradiation. By E17 the ectopic cell masses formed so as to replace the parts of the ventricular zone where no anti-MK immunoreactive radial fibers were present, but where anti-GFAP-stained fibrillary astrocytes emerged in the ectopic cell masses from the early postnatal period. The results suggested a twofold source of the generated astrocytes: either directly from a separate precursor of the astrocytes, or due to the transformation of the classic radial glial cells. In the newborn, numerous protoplasmic transitional forms displaced by astrocytes in irradiated brains indicated that reactive gliosis was a powerful response of a brain exposed to irradiation.

Published
1997
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40. Follow-up Study on Histogenesis of Microcephaly Associated with Ectopic Gray Matter Induced by Prenatal {gamma}-lrradiation in the Mouse

Author

Sun, Xue-Zhi, Inouye, Minoru, Takagishi, Yoshiko, Hayasaka, Shizu, and Yamamura, Hideki

Abstract

Brain malformation with ectopic gray matter was visualized with magnetic resonance imaging in small-sized heads of prenatally exposed atomic bomb survivors. The identical brain malformation was reproduced in mice and its histogenesis was studied in the present experiment. Pregnant mice were exposed to 60Co γ-irradiation at a single dose of 1.5 Gy on embryonic day 13 (E13), and then injected intraperitoneally with 30 mg/kg BrdU on E15. The extensive dead cells appeared throughout the brain mantle at 6 hours (h) after exposure. On E16 cell aggregations formed rosettes. On El8 a high proportion of BrdU-labeled cells reached the superficial layers of the cortical plate with the remaining cells located in the ectopic neuronal masses. The quantitative study showed that labeled cells in layers II to III were fewer and those in layers IV to VI more numerous in the prenatally irradiated adult mice than in controls. The anti-GFAP immunostaining revealed that the glial fibers in the irradiated mice were preserved, but disorganized. These findings suggested that the majority of migrating neurons were able to arrive at their normal layers, but some neurons remained due to the interrupted migratory pathway and eventually formed ectopic neuronal masses beneath the subcortical white matter.

Published
1996
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41. Animal models of xeroderma pigmentosum.

Author

Sun XZ, Zhang R, Cui C, Harada YN, Hisano S, Gu Y, Fukui Y, and Yonehara H

Subjects
Animals, Humans, Xeroderma Pigmentosum metabolism, DNA Repair, Disease Models, Animal, Xeroderma Pigmentosum genetics
Published
2008
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42. Normal and abnormal neuronal migration in the developing cerebral cortex.

Author

Sun XZ, Takahashi S, Cui C, Zhang R, Sakata-Haga H, Sawada K, and Fukui Y

Subjects
1-Alkyl-2-acetylglycerophosphocholine Esterase, Animals, Biomarkers, Carrier Proteins analysis, Cell Adhesion Molecules, Neuronal deficiency, Cell Adhesion Molecules, Neuronal genetics, Cell Adhesion Molecules, Neuronal physiology, Cerebral Cortex abnormalities, Cerebral Cortex embryology, Cerebral Cortex growth & development, Extracellular Matrix Proteins deficiency, Extracellular Matrix Proteins genetics, Extracellular Matrix Proteins physiology, Female, Humans, Male, Mammals anatomy & histology, Mammals embryology, Mice, Mice, Neurologic Mutants, Microcephaly genetics, Microcephaly pathology, Microtubule-Associated Proteins deficiency, Microtubule-Associated Proteins genetics, Microtubule-Associated Proteins physiology, Midkine, Models, Animal, Morphogenesis, Nerve Tissue Proteins deficiency, Nerve Tissue Proteins genetics, Nerve Tissue Proteins physiology, Neuroglia physiology, Pregnancy, Rats, Reelin Protein, Serine Endopeptidases, Syndrome, Teratogens toxicity, X Chromosome genetics, Zellweger Syndrome genetics, Zellweger Syndrome pathology, Cell Movement, Cerebral Cortex cytology, Cytokines, Neurons cytology
Abstract

Neuronal migration is the critical cellular process which initiates histogenesis of cerebral cortex. Migration involves a series of complex cell interactions and transformation. After completing their final mitosis, neurons migrate from the ventricular zone into the cortical plate, and then establish neuronal lamina and settle onto the outermost layer, forming an "inside-out" gradient of maturation. This process is guided by radial glial fibers, requires proper receptors, ligands, other unknown extracellular factors, and local signaling to stop neuronal migration. This process is also highly sensitive to various physical, chemical and biological agents as well as to genetic mutations. Any disturbance of the normal process may result in neuronal migration disorder. Such neuronal migration disorder is believed as major cause of both gross brain malformation and more special cerebral structural and functional abnormalities in experimental animals and in humans. An increasing number of instructive studies on experimental models and several genetic model systems of neuronal migration disorder have established the foundation of cortex formation and provided deeper insights into the genetic and molecular mechanisms underlying normal and abnormal neuronal migration.

Published
2002

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