The Experts below are selected from a list of 216 Experts worldwide ranked by ideXlab platform
Masato Nose - One of the best experts on this subject based on the ideXlab platform.
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genome analysis of collagen disease in mrl lpr mice Polygenic Inheritance resulting in the complex pathological manifestations
International Journal of Cardiology, 2000Co-Authors: Masato Nose, Miyuki Nishihara, Miho Terada, Junji Kamogawa, Shiro Mori, Tatsuhiko Miyazaki, Weimin Qu, Syuichi NakatsuruAbstract:Abstract MRL/MpJ- lpr / lpr (MRL/lpr) mice develop collagen disease involving vasculitis, glomerulonephritis, arthritis and sialoadenitis, each of which has been studied as a model for polyarteritis, lupus nephritis, rheumatoid arthritis and Sjogren's syndrome, respectively. In the previous studies, we observed genetic segregation of these complex pathological manifestations throughout the genome recombination with a C57Bl/6- lpr / lpr or a C3H/HeJ- lpr / lpr (C3H/lpr) strain of mice which rarely develops such lesions, indicating that development of collagen disease is dependent on an MRL host genetic background. To clarify the mode of Inheritance and the gene loci affecting four types of the lesions in MRL/lpr mice; vasculitis, glomerulonephritis, arthritis and sialoadenitis, a genetic dissection of the lesions was carried out by using MRL/lpr, C3H/lpr, (MRL/lpr×C3H/lpr) F1 intercross, and MRL/lpr×(MRL/lpr×C3H/lpr) F1 backcross mice. Definition of each lesion was performed by histopathology under light microscopy, and genomic DNA of the backcross mice were subjected to association studies by chi-square analysis for determining which polymorphic microsatellite locus occurs at higher frequency among affected compared to unaffected individuals for each lesion. We observed that gene loci recessively associated with each lesion were mapped on different chromosomal positions. We conclude that each of four types of the lesions in MRL/lpr mice is under the control of different set of genes, suggesting the complex pathological manifestations of collagen disease result from Polygenic Inheritance.
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genetic basis of autoimmune sialadenitis in mrl lpr lupus prone mice additive and hierarchical properties of Polygenic Inheritance
Arthritis & Rheumatism, 1999Co-Authors: Miyuki Nishihara, Miho Terada, Junji Kamogawa, Yuichi Ohashi, Shiro Mori, Shuichi Nakatsuru, Yusuke Nakamura, Masato NoseAbstract:Objective. To clarify the mode of Inheritance of autoimmune sialadenitis in MRL/MpJ-lpr/lpr (MRL/ lpr) lupus-prone mice and identify the susceptibility loci. Methods. MRL/lpr, C3H/HeJ-lpr/lpr (C3H/lpr), (MRL/lpr × C3H/lpr)F 1 intercross, and MRL/lpr × (MRL/lpr × C3H/lpr)F 1 backcross mice were prepared, and sialadenitis in individual mice was analyzed by histopathologic grading. The genomic DNA of the backcross mice was examined by simple sequence-length polymorphism analysis, and the highly associated polymorphic microsatellite markers with sialadenitis were determined as sialadenitis susceptibility loci. Results. Four susceptible gene loci recessively associated with sialadenitis were mapped on chromosomes 10, 18, 4, and 1, respectively. These loci manifested additive and hierarchical properties in the development of sialadenitis. Conclusion. The results indicate that sialadenitis in MRL/lpr mice is under the control of Polygenic Inheritance, possibly involving allelic polymorphism.
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Genetic basis of autoimmune sialadenitis in MRL/lpr lupus-prone mice: Additive and hierarchical properties of Polygenic Inheritance
Arthritis & Rheumatism, 1999Co-Authors: Miyuki Nishihara, Miho Terada, Junji Kamogawa, Yuichi Ohashi, Shiro Mori, Shuichi Nakatsuru, Yusuke Nakamura, Masato NoseAbstract:Objective. To clarify the mode of Inheritance of autoimmune sialadenitis in MRL/MpJ-lpr/lpr (MRL/ lpr) lupus-prone mice and identify the susceptibility loci. Methods. MRL/lpr, C3H/HeJ-lpr/lpr (C3H/lpr), (MRL/lpr × C3H/lpr)F 1 intercross, and MRL/lpr × (MRL/lpr × C3H/lpr)F 1 backcross mice were prepared, and sialadenitis in individual mice was analyzed by histopathologic grading. The genomic DNA of the backcross mice was examined by simple sequence-length polymorphism analysis, and the highly associated polymorphic microsatellite markers with sialadenitis were determined as sialadenitis susceptibility loci. Results. Four susceptible gene loci recessively associated with sialadenitis were mapped on chromosomes 10, 18, 4, and 1, respectively. These loci manifested additive and hierarchical properties in the development of sialadenitis. Conclusion. The results indicate that sialadenitis in MRL/lpr mice is under the control of Polygenic Inheritance, possibly involving allelic polymorphism.
Miyuki Nishihara - One of the best experts on this subject based on the ideXlab platform.
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genome analysis of collagen disease in mrl lpr mice Polygenic Inheritance resulting in the complex pathological manifestations
International Journal of Cardiology, 2000Co-Authors: Masato Nose, Miyuki Nishihara, Miho Terada, Junji Kamogawa, Shiro Mori, Tatsuhiko Miyazaki, Weimin Qu, Syuichi NakatsuruAbstract:Abstract MRL/MpJ- lpr / lpr (MRL/lpr) mice develop collagen disease involving vasculitis, glomerulonephritis, arthritis and sialoadenitis, each of which has been studied as a model for polyarteritis, lupus nephritis, rheumatoid arthritis and Sjogren's syndrome, respectively. In the previous studies, we observed genetic segregation of these complex pathological manifestations throughout the genome recombination with a C57Bl/6- lpr / lpr or a C3H/HeJ- lpr / lpr (C3H/lpr) strain of mice which rarely develops such lesions, indicating that development of collagen disease is dependent on an MRL host genetic background. To clarify the mode of Inheritance and the gene loci affecting four types of the lesions in MRL/lpr mice; vasculitis, glomerulonephritis, arthritis and sialoadenitis, a genetic dissection of the lesions was carried out by using MRL/lpr, C3H/lpr, (MRL/lpr×C3H/lpr) F1 intercross, and MRL/lpr×(MRL/lpr×C3H/lpr) F1 backcross mice. Definition of each lesion was performed by histopathology under light microscopy, and genomic DNA of the backcross mice were subjected to association studies by chi-square analysis for determining which polymorphic microsatellite locus occurs at higher frequency among affected compared to unaffected individuals for each lesion. We observed that gene loci recessively associated with each lesion were mapped on different chromosomal positions. We conclude that each of four types of the lesions in MRL/lpr mice is under the control of different set of genes, suggesting the complex pathological manifestations of collagen disease result from Polygenic Inheritance.
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genetic basis of autoimmune sialadenitis in mrl lpr lupus prone mice additive and hierarchical properties of Polygenic Inheritance
Arthritis & Rheumatism, 1999Co-Authors: Miyuki Nishihara, Miho Terada, Junji Kamogawa, Yuichi Ohashi, Shiro Mori, Shuichi Nakatsuru, Yusuke Nakamura, Masato NoseAbstract:Objective. To clarify the mode of Inheritance of autoimmune sialadenitis in MRL/MpJ-lpr/lpr (MRL/ lpr) lupus-prone mice and identify the susceptibility loci. Methods. MRL/lpr, C3H/HeJ-lpr/lpr (C3H/lpr), (MRL/lpr × C3H/lpr)F 1 intercross, and MRL/lpr × (MRL/lpr × C3H/lpr)F 1 backcross mice were prepared, and sialadenitis in individual mice was analyzed by histopathologic grading. The genomic DNA of the backcross mice was examined by simple sequence-length polymorphism analysis, and the highly associated polymorphic microsatellite markers with sialadenitis were determined as sialadenitis susceptibility loci. Results. Four susceptible gene loci recessively associated with sialadenitis were mapped on chromosomes 10, 18, 4, and 1, respectively. These loci manifested additive and hierarchical properties in the development of sialadenitis. Conclusion. The results indicate that sialadenitis in MRL/lpr mice is under the control of Polygenic Inheritance, possibly involving allelic polymorphism.
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Genetic basis of autoimmune sialadenitis in MRL/lpr lupus-prone mice: Additive and hierarchical properties of Polygenic Inheritance
Arthritis & Rheumatism, 1999Co-Authors: Miyuki Nishihara, Miho Terada, Junji Kamogawa, Yuichi Ohashi, Shiro Mori, Shuichi Nakatsuru, Yusuke Nakamura, Masato NoseAbstract:Objective. To clarify the mode of Inheritance of autoimmune sialadenitis in MRL/MpJ-lpr/lpr (MRL/ lpr) lupus-prone mice and identify the susceptibility loci. Methods. MRL/lpr, C3H/HeJ-lpr/lpr (C3H/lpr), (MRL/lpr × C3H/lpr)F 1 intercross, and MRL/lpr × (MRL/lpr × C3H/lpr)F 1 backcross mice were prepared, and sialadenitis in individual mice was analyzed by histopathologic grading. The genomic DNA of the backcross mice was examined by simple sequence-length polymorphism analysis, and the highly associated polymorphic microsatellite markers with sialadenitis were determined as sialadenitis susceptibility loci. Results. Four susceptible gene loci recessively associated with sialadenitis were mapped on chromosomes 10, 18, 4, and 1, respectively. These loci manifested additive and hierarchical properties in the development of sialadenitis. Conclusion. The results indicate that sialadenitis in MRL/lpr mice is under the control of Polygenic Inheritance, possibly involving allelic polymorphism.
Shiro Mori - One of the best experts on this subject based on the ideXlab platform.
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genome analysis of collagen disease in mrl lpr mice Polygenic Inheritance resulting in the complex pathological manifestations
International Journal of Cardiology, 2000Co-Authors: Masato Nose, Miyuki Nishihara, Miho Terada, Junji Kamogawa, Shiro Mori, Tatsuhiko Miyazaki, Weimin Qu, Syuichi NakatsuruAbstract:Abstract MRL/MpJ- lpr / lpr (MRL/lpr) mice develop collagen disease involving vasculitis, glomerulonephritis, arthritis and sialoadenitis, each of which has been studied as a model for polyarteritis, lupus nephritis, rheumatoid arthritis and Sjogren's syndrome, respectively. In the previous studies, we observed genetic segregation of these complex pathological manifestations throughout the genome recombination with a C57Bl/6- lpr / lpr or a C3H/HeJ- lpr / lpr (C3H/lpr) strain of mice which rarely develops such lesions, indicating that development of collagen disease is dependent on an MRL host genetic background. To clarify the mode of Inheritance and the gene loci affecting four types of the lesions in MRL/lpr mice; vasculitis, glomerulonephritis, arthritis and sialoadenitis, a genetic dissection of the lesions was carried out by using MRL/lpr, C3H/lpr, (MRL/lpr×C3H/lpr) F1 intercross, and MRL/lpr×(MRL/lpr×C3H/lpr) F1 backcross mice. Definition of each lesion was performed by histopathology under light microscopy, and genomic DNA of the backcross mice were subjected to association studies by chi-square analysis for determining which polymorphic microsatellite locus occurs at higher frequency among affected compared to unaffected individuals for each lesion. We observed that gene loci recessively associated with each lesion were mapped on different chromosomal positions. We conclude that each of four types of the lesions in MRL/lpr mice is under the control of different set of genes, suggesting the complex pathological manifestations of collagen disease result from Polygenic Inheritance.
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genetic basis of autoimmune sialadenitis in mrl lpr lupus prone mice additive and hierarchical properties of Polygenic Inheritance
Arthritis & Rheumatism, 1999Co-Authors: Miyuki Nishihara, Miho Terada, Junji Kamogawa, Yuichi Ohashi, Shiro Mori, Shuichi Nakatsuru, Yusuke Nakamura, Masato NoseAbstract:Objective. To clarify the mode of Inheritance of autoimmune sialadenitis in MRL/MpJ-lpr/lpr (MRL/ lpr) lupus-prone mice and identify the susceptibility loci. Methods. MRL/lpr, C3H/HeJ-lpr/lpr (C3H/lpr), (MRL/lpr × C3H/lpr)F 1 intercross, and MRL/lpr × (MRL/lpr × C3H/lpr)F 1 backcross mice were prepared, and sialadenitis in individual mice was analyzed by histopathologic grading. The genomic DNA of the backcross mice was examined by simple sequence-length polymorphism analysis, and the highly associated polymorphic microsatellite markers with sialadenitis were determined as sialadenitis susceptibility loci. Results. Four susceptible gene loci recessively associated with sialadenitis were mapped on chromosomes 10, 18, 4, and 1, respectively. These loci manifested additive and hierarchical properties in the development of sialadenitis. Conclusion. The results indicate that sialadenitis in MRL/lpr mice is under the control of Polygenic Inheritance, possibly involving allelic polymorphism.
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Genetic basis of autoimmune sialadenitis in MRL/lpr lupus-prone mice: Additive and hierarchical properties of Polygenic Inheritance
Arthritis & Rheumatism, 1999Co-Authors: Miyuki Nishihara, Miho Terada, Junji Kamogawa, Yuichi Ohashi, Shiro Mori, Shuichi Nakatsuru, Yusuke Nakamura, Masato NoseAbstract:Objective. To clarify the mode of Inheritance of autoimmune sialadenitis in MRL/MpJ-lpr/lpr (MRL/ lpr) lupus-prone mice and identify the susceptibility loci. Methods. MRL/lpr, C3H/HeJ-lpr/lpr (C3H/lpr), (MRL/lpr × C3H/lpr)F 1 intercross, and MRL/lpr × (MRL/lpr × C3H/lpr)F 1 backcross mice were prepared, and sialadenitis in individual mice was analyzed by histopathologic grading. The genomic DNA of the backcross mice was examined by simple sequence-length polymorphism analysis, and the highly associated polymorphic microsatellite markers with sialadenitis were determined as sialadenitis susceptibility loci. Results. Four susceptible gene loci recessively associated with sialadenitis were mapped on chromosomes 10, 18, 4, and 1, respectively. These loci manifested additive and hierarchical properties in the development of sialadenitis. Conclusion. The results indicate that sialadenitis in MRL/lpr mice is under the control of Polygenic Inheritance, possibly involving allelic polymorphism.
Junji Kamogawa - One of the best experts on this subject based on the ideXlab platform.
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genome analysis of collagen disease in mrl lpr mice Polygenic Inheritance resulting in the complex pathological manifestations
International Journal of Cardiology, 2000Co-Authors: Masato Nose, Miyuki Nishihara, Miho Terada, Junji Kamogawa, Shiro Mori, Tatsuhiko Miyazaki, Weimin Qu, Syuichi NakatsuruAbstract:Abstract MRL/MpJ- lpr / lpr (MRL/lpr) mice develop collagen disease involving vasculitis, glomerulonephritis, arthritis and sialoadenitis, each of which has been studied as a model for polyarteritis, lupus nephritis, rheumatoid arthritis and Sjogren's syndrome, respectively. In the previous studies, we observed genetic segregation of these complex pathological manifestations throughout the genome recombination with a C57Bl/6- lpr / lpr or a C3H/HeJ- lpr / lpr (C3H/lpr) strain of mice which rarely develops such lesions, indicating that development of collagen disease is dependent on an MRL host genetic background. To clarify the mode of Inheritance and the gene loci affecting four types of the lesions in MRL/lpr mice; vasculitis, glomerulonephritis, arthritis and sialoadenitis, a genetic dissection of the lesions was carried out by using MRL/lpr, C3H/lpr, (MRL/lpr×C3H/lpr) F1 intercross, and MRL/lpr×(MRL/lpr×C3H/lpr) F1 backcross mice. Definition of each lesion was performed by histopathology under light microscopy, and genomic DNA of the backcross mice were subjected to association studies by chi-square analysis for determining which polymorphic microsatellite locus occurs at higher frequency among affected compared to unaffected individuals for each lesion. We observed that gene loci recessively associated with each lesion were mapped on different chromosomal positions. We conclude that each of four types of the lesions in MRL/lpr mice is under the control of different set of genes, suggesting the complex pathological manifestations of collagen disease result from Polygenic Inheritance.
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genetic basis of autoimmune sialadenitis in mrl lpr lupus prone mice additive and hierarchical properties of Polygenic Inheritance
Arthritis & Rheumatism, 1999Co-Authors: Miyuki Nishihara, Miho Terada, Junji Kamogawa, Yuichi Ohashi, Shiro Mori, Shuichi Nakatsuru, Yusuke Nakamura, Masato NoseAbstract:Objective. To clarify the mode of Inheritance of autoimmune sialadenitis in MRL/MpJ-lpr/lpr (MRL/ lpr) lupus-prone mice and identify the susceptibility loci. Methods. MRL/lpr, C3H/HeJ-lpr/lpr (C3H/lpr), (MRL/lpr × C3H/lpr)F 1 intercross, and MRL/lpr × (MRL/lpr × C3H/lpr)F 1 backcross mice were prepared, and sialadenitis in individual mice was analyzed by histopathologic grading. The genomic DNA of the backcross mice was examined by simple sequence-length polymorphism analysis, and the highly associated polymorphic microsatellite markers with sialadenitis were determined as sialadenitis susceptibility loci. Results. Four susceptible gene loci recessively associated with sialadenitis were mapped on chromosomes 10, 18, 4, and 1, respectively. These loci manifested additive and hierarchical properties in the development of sialadenitis. Conclusion. The results indicate that sialadenitis in MRL/lpr mice is under the control of Polygenic Inheritance, possibly involving allelic polymorphism.
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Genetic basis of autoimmune sialadenitis in MRL/lpr lupus-prone mice: Additive and hierarchical properties of Polygenic Inheritance
Arthritis & Rheumatism, 1999Co-Authors: Miyuki Nishihara, Miho Terada, Junji Kamogawa, Yuichi Ohashi, Shiro Mori, Shuichi Nakatsuru, Yusuke Nakamura, Masato NoseAbstract:Objective. To clarify the mode of Inheritance of autoimmune sialadenitis in MRL/MpJ-lpr/lpr (MRL/ lpr) lupus-prone mice and identify the susceptibility loci. Methods. MRL/lpr, C3H/HeJ-lpr/lpr (C3H/lpr), (MRL/lpr × C3H/lpr)F 1 intercross, and MRL/lpr × (MRL/lpr × C3H/lpr)F 1 backcross mice were prepared, and sialadenitis in individual mice was analyzed by histopathologic grading. The genomic DNA of the backcross mice was examined by simple sequence-length polymorphism analysis, and the highly associated polymorphic microsatellite markers with sialadenitis were determined as sialadenitis susceptibility loci. Results. Four susceptible gene loci recessively associated with sialadenitis were mapped on chromosomes 10, 18, 4, and 1, respectively. These loci manifested additive and hierarchical properties in the development of sialadenitis. Conclusion. The results indicate that sialadenitis in MRL/lpr mice is under the control of Polygenic Inheritance, possibly involving allelic polymorphism.
Miho Terada - One of the best experts on this subject based on the ideXlab platform.
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genome analysis of collagen disease in mrl lpr mice Polygenic Inheritance resulting in the complex pathological manifestations
International Journal of Cardiology, 2000Co-Authors: Masato Nose, Miyuki Nishihara, Miho Terada, Junji Kamogawa, Shiro Mori, Tatsuhiko Miyazaki, Weimin Qu, Syuichi NakatsuruAbstract:Abstract MRL/MpJ- lpr / lpr (MRL/lpr) mice develop collagen disease involving vasculitis, glomerulonephritis, arthritis and sialoadenitis, each of which has been studied as a model for polyarteritis, lupus nephritis, rheumatoid arthritis and Sjogren's syndrome, respectively. In the previous studies, we observed genetic segregation of these complex pathological manifestations throughout the genome recombination with a C57Bl/6- lpr / lpr or a C3H/HeJ- lpr / lpr (C3H/lpr) strain of mice which rarely develops such lesions, indicating that development of collagen disease is dependent on an MRL host genetic background. To clarify the mode of Inheritance and the gene loci affecting four types of the lesions in MRL/lpr mice; vasculitis, glomerulonephritis, arthritis and sialoadenitis, a genetic dissection of the lesions was carried out by using MRL/lpr, C3H/lpr, (MRL/lpr×C3H/lpr) F1 intercross, and MRL/lpr×(MRL/lpr×C3H/lpr) F1 backcross mice. Definition of each lesion was performed by histopathology under light microscopy, and genomic DNA of the backcross mice were subjected to association studies by chi-square analysis for determining which polymorphic microsatellite locus occurs at higher frequency among affected compared to unaffected individuals for each lesion. We observed that gene loci recessively associated with each lesion were mapped on different chromosomal positions. We conclude that each of four types of the lesions in MRL/lpr mice is under the control of different set of genes, suggesting the complex pathological manifestations of collagen disease result from Polygenic Inheritance.
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genetic basis of autoimmune sialadenitis in mrl lpr lupus prone mice additive and hierarchical properties of Polygenic Inheritance
Arthritis & Rheumatism, 1999Co-Authors: Miyuki Nishihara, Miho Terada, Junji Kamogawa, Yuichi Ohashi, Shiro Mori, Shuichi Nakatsuru, Yusuke Nakamura, Masato NoseAbstract:Objective. To clarify the mode of Inheritance of autoimmune sialadenitis in MRL/MpJ-lpr/lpr (MRL/ lpr) lupus-prone mice and identify the susceptibility loci. Methods. MRL/lpr, C3H/HeJ-lpr/lpr (C3H/lpr), (MRL/lpr × C3H/lpr)F 1 intercross, and MRL/lpr × (MRL/lpr × C3H/lpr)F 1 backcross mice were prepared, and sialadenitis in individual mice was analyzed by histopathologic grading. The genomic DNA of the backcross mice was examined by simple sequence-length polymorphism analysis, and the highly associated polymorphic microsatellite markers with sialadenitis were determined as sialadenitis susceptibility loci. Results. Four susceptible gene loci recessively associated with sialadenitis were mapped on chromosomes 10, 18, 4, and 1, respectively. These loci manifested additive and hierarchical properties in the development of sialadenitis. Conclusion. The results indicate that sialadenitis in MRL/lpr mice is under the control of Polygenic Inheritance, possibly involving allelic polymorphism.
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Genetic basis of autoimmune sialadenitis in MRL/lpr lupus-prone mice: Additive and hierarchical properties of Polygenic Inheritance
Arthritis & Rheumatism, 1999Co-Authors: Miyuki Nishihara, Miho Terada, Junji Kamogawa, Yuichi Ohashi, Shiro Mori, Shuichi Nakatsuru, Yusuke Nakamura, Masato NoseAbstract:Objective. To clarify the mode of Inheritance of autoimmune sialadenitis in MRL/MpJ-lpr/lpr (MRL/ lpr) lupus-prone mice and identify the susceptibility loci. Methods. MRL/lpr, C3H/HeJ-lpr/lpr (C3H/lpr), (MRL/lpr × C3H/lpr)F 1 intercross, and MRL/lpr × (MRL/lpr × C3H/lpr)F 1 backcross mice were prepared, and sialadenitis in individual mice was analyzed by histopathologic grading. The genomic DNA of the backcross mice was examined by simple sequence-length polymorphism analysis, and the highly associated polymorphic microsatellite markers with sialadenitis were determined as sialadenitis susceptibility loci. Results. Four susceptible gene loci recessively associated with sialadenitis were mapped on chromosomes 10, 18, 4, and 1, respectively. These loci manifested additive and hierarchical properties in the development of sialadenitis. Conclusion. The results indicate that sialadenitis in MRL/lpr mice is under the control of Polygenic Inheritance, possibly involving allelic polymorphism.