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The Senescence-Accelerated Mouse (SAM): An Animal Model of Senescence
Proceedings of the 2nd International Conference on Senescene: The SAM Model, Sapporo, Japan 21-23 July 2003, ICS 1260
9780444514134
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Description
This volume represents a summary of reports on studies using the Senescence Accelerated Mouse, as presented at the 2nd International Conference on Senescence:: The SAM Model, held from 21-23 July in Sapporo, Japan.
Work on the SAM began in 1968 in the Department of Pathology, Chart Disease Research Institute (currently Field of Regeneration Control Institute for Frontier Medical Sciences) of Kyoto University. Since 1982, experiments on the SAM have been carried out in over 300 laboratories in Japan and other countries.
Many emerging aspects of the SAM model were successfully dealt with at the first conference, which was held in 1994 in Kyoto. Dramatic progress in research on the SAM model has been made since. The focus of this conference was on findings obtained by using the SAM model and pertinent information was provided by investigators working on the SAM model together with comments for those who are about to embark on SAM-related investigations.
Many excellent papers included in this issue offer new insights into the significance of the SAM as an animal model of aging.
Work on the SAM began in 1968 in the Department of Pathology, Chart Disease Research Institute (currently Field of Regeneration Control Institute for Frontier Medical Sciences) of Kyoto University. Since 1982, experiments on the SAM have been carried out in over 300 laboratories in Japan and other countries.
Many emerging aspects of the SAM model were successfully dealt with at the first conference, which was held in 1994 in Kyoto. Dramatic progress in research on the SAM model has been made since. The focus of this conference was on findings obtained by using the SAM model and pertinent information was provided by investigators working on the SAM model together with comments for those who are about to embark on SAM-related investigations.
Many excellent papers included in this issue offer new insights into the significance of the SAM as an animal model of aging.
Product Details
48093
9780444514134
9780444514134
Data sheet
- Publication date
- 2004
- Issue number
- 1
- Cover
- hard cover
- Pages count
- 464
- Weight (g)
- 989
- Preface.
Plenary lectures.
Effects of environment on life span and pathobiological phenotypes in senescence-accelerated mice (T. Takeda). Caloric restriction, gene expression and aging (R. Weindruch).
New frontiers in SAM research.
The SAMP8 mouse as a model for Alzheimer disease: studies from Saint Louis University (J.E. Morley et al.). Quantitative trait loci (QTL) for age-related memory dysfunction in SAMP8 and JF1mice (M. Isobe et al.). Mouse senile amyloidosis in the SAM model (K. Higuchi et al.). Immune system deficiencies in SAM (T. Hosokawa). Mitochondrial dysfunction and an impaired response to higher oxidative status accelerate cellular aging in SAMP strains of mice (M. Hosokawa).
Etiopathogenesis of SAMP6 senile osteoporosis.
Age-related bone loss: lessons from the osteoporotic SAMP6 mouse model (R.L. Jilka, R.J.S. Reis, S.C. Manolagas). Reduced AP-1 mediated transcription of interleukin-11 gene in marrow stromal cells as a mechanism of senile Osteoprosis: lessons from SAMP6 (D. Inoue, T. Matsumoto).
Neuroscience in aging and SAM research.
Pathobiological features in neurodegenerative diseases: an overview (M. Higuchi, J.Q. Trojanowski, V.M. Lee). Pathological studies of neurodegeneration in SAMP10 mice (A. Shimada et al.). Altered Gene expression in the brain of senescence accelerated mouse SAMP8 (R. Takahashi, S. Goto). Biochemical changes in the brain of the senescence-accelerated mouse (SAM) P8 and P10 (Y. Nomura et al.). Emotional disorders and memory deficits in senescence-accelerated mice, SAMP8 and SAMP10 (M. Miyamoto).
Modulation of accelerated senescence and age-associated pathologies in SAM.
Chemical intervention in senescence accelerated mice metabolism for modeling neurodegenerative diseases: an overview (A. Boldyrev et al.). Prevention and treatment of age-associated disease in SAM by bone marrow transplantation with or without thymus grafts (M. Inaba, H. Iwai, S. Ikehara). Ameliorative effects of acetyl-L-carnitine and acidic fibroblast growth factor fragment analog on brain lipid hydroperoxide level, passive avoidance learning, and/or immunoreactivity for choline acetyltransferase in the medial septum in senescence-accelerated mice (K. Sasaki et al.). Ameliorative effects of dietary carotenoids on memory deficits in senescence-accelerated mice (SAMP8) (H. Suganuma et al.). The roles of enteric bacteria on the development of Chrons disease like intestinal inflammation in SAMP1/Yit mice (S. Matsumoto). Ameliorative effects of nucleosides on senescence accelaration and memory deterioration in senescence-accelerated mice (D. Kunii et al.).
Practical application in the breeding and experiments of SAM.
Breeding system and background data for SAM mice at Japan SLC (T. Suzuki et al.). Application of the passive avoidance task for manitenance and breeding of SAMP8/Ta to maintain stable phenotype (T. Abe, Y. Omori). Effects of housing and nutrition condition on the reproduction of SAMR1, SAMP6 and SAMP8 at NILS aging farm (S. Tanaka, K. Shiokawa, O. Miyaishi). Homepage of the council for SAM research ( http://samrcmd.shinshu-u.ac.jp) (J. Sawashita et al.). Abnormal accumulation of corpora lutea in ovaries of the senescence accelerated mouse prone (SAMP) (N. Manabe et al.). Genetic monitoring system for SAM strains utilizing DNA markers (M. Mori, K. Higuchi). Physiological characteristics in SAMP1 and SAMP2 mice (Y. Yanagidaira, K. Higuchi).
Immunology and senescence.
Morphological changes of the thymus under stress caused by water immersion and restraint in SAMP1 mice (M.S. Miyamoto, Y. Miyamoto, T. Hosokawa). Regulatory effects of noradrenaline and corticosterone on the antibody-forming response of cultured spleen cells from SAMP1 mice (M. Kitamura, Y. Yagi, T. Hosokawa). Antibody-forming response of cultured spleen cells to a protein antigen: function of antigen presenting cells in SAMP1 mice (T. Kimura, A. Kohdan, T. Hosokawa). Regulatory effects of noradrenaline on the production of Th1 and Th2 cytokines by cultured spleen cells in SAMP1 mice (S. Hashimoto, R. Naruse, T. Hosokawa). The stability of interleukin-2 mRNA transcribed in splenic CD4+ T cells from SAMP1 mice (Y. Nishimura et al.).
Endocrinology and senescence.
Expression of matrix metalloproteinases and their tissue inhibitors in ovaries of senescence accelerated mice (M. Shimabe et al.). Expression of prolactin receptor mRNAs in ovaries of senescence accelerated mice (M. Kiso et al.). Age-related changes of the hippocampal estrogen receptor gene expression in senescence-accelerated mouse (W. Zhou et al.).
Oxidative stress and senescence.
Production of reactive oxygen species by cerebellum granule cells isolated from senescence accelerated mice (V. Kazey, E. Tuneva, A. Boldyrev). Analysis of the oxidative stress state in the brain and peripheral organs of senescence-accelerated mouse (SAM) model (S. Matsugo, F. Yasui, K. Sasaki). Mitochondrial alterations and a higher oxidative status in cultured fibroblast-like cells from senescence-accelerated mice (Y. Chiba et al.). Age-related changes in the oxidation-reduction characteristics and the 8-OHdG accumulation in liver, lung, brain of SAMP1 and SAMR1 (F. Maehira et al.).
Neurodegeneration.
Microglial activation around amyloid-â deposits in mouse and rat models (K. Takata et al.). Clearance of amyloid-â in microglial culture model (D. Tsuchiya et al.). Neuroprotection against focal ischemia in the hyperbilirubinemic rat model (T. Sugisaki et al.). Hemiparkinsonian rat models: different sensitivity of dopaminergic neurotoxins (J. Kondo et al.). In vitro neurodegeneration model: dopaminergic toxin-induced apoptosis in human SH-SY5Y cells (K. Nakamura et al.). Parkinsonian model of planarian, an invertebrate flatworm (M. Inden et al.).
Neuronal and behavioral disorder in senescence.
Accelerated senescence and adaptation to cold exposure (Y. Yamashita et al.). Involvement of the glutamatergic system in behavioral disorders in senescence-accelerated mice (SAMP8) (Y. Fujiwara et al.). Age-related decrease in spontaneity observed in senescence-accelerated mice (SAMP10) and the involvement of the dopaminergic system in behavioral disorders (H. Takahashi et al.). Effects of rearing conditions on aging characteristics and pathobiological phenotypes in SAMP10 mice (M. Kikumori et al.). Age-related changes in hippocampal theta rhythm in SAMP8 mouse (A. Sano et al.). Deterioration in synaptic plasticity of cultured hippocampal neurons of senescence-accelerated mouse prone 8 (S. Yang et al.). Age-related changes in telomere of brain cell in aging SAMP10 mice (S. Wang et al.). Centripetal retraction of dendrites with apical vulnerability in the prefrontal neurons of aged SAMP10 mice (H. Keino et al.). Age-related changes in blood-brain barrier of the SAM brain (M. Ueno et al.). Developmentally retarded expression of the glial glutamate transporter, GLT-1, in the cerebral cortex of senescence-accelerated prone mouse SAMP8 (T. Kurokawa et al.).
Genetical and molecular aspect of senescence.
Genetic study of learning and memory deficits in SAMP8 mice (K. Tomobe et al.). Relationship between immune activity, senile amyloidosis and life span of hybrids of SAMP1 and B10.BR mice (E. Toichi et al.). Microarray analysis of mRNA expressed in colon of senescence-accelerated mouse (SAM)P6 (T. Kawashima, Y. Shidoji, T. Oku). Expression of a novel gene containing ankyrin-repeat in SAMP8 mouse hippocampus (N. Yamamura et al.). Seeking for ageing-associated gene expression in cerebral tissue of senescence-accelerated mouse (SAM) (C. Zhang, J. Cheng, Q. Chen). Aging and acupuncture effects on hippocampal gene expression profile of SAMP10 (J. Han et al.). Induction of AApoAII and AA amyloidosis by the injections of various amyloid fibrils (X. Fu et al.). Senescence-accelerated mouse accumulates dietary triacylglycerols in the intestinal mucosa with aging (S. Nishizono, A. Ogawa, K. Imaizumi).
Amelioration of senile acceleration.
Prevention of senile osteoporosis in SAMP6 mice by intra-bone marrow injection of allogeneic bone marrow cells (K. Takada et al.). Effects of Ganoderma on aging and learning and memory ability in senescence accelerated mice (M.-F. Wang et al.). Neuroprotective effect of magnolol in the hippocampus of senescence-accelerated mice (SAMP1) (M. Akagi et al.). Improvement in brain function and oxidative damage of aged senescence-accelerated mice (SAMP10) by green tea catechins (K. Unno, F. Takabayashi, N. Oku). Effects of red algae cultivated with deep-sea water on the oxidation-reduction status of liver, lung, brain, and bone metabolism in SAMP1 and SAMR1 (F. Maehira et al.). Influence of a change in the synovia constituent on temporomandibular joint in senescence accelerated mouse P8 (T. Yokoyama et al.). Effect of Liuwei Dihuang decoction on the function of hypothalamus-pituitary-ovary axis in senescence-accelerated mouse (Y. Zhang et al.). Effects of dietary fats on senile amyloidosis in SAMP1 mice (M. Umezawa et al.). Characteristics of heme biosynthesis in the liver of the senescence-accelerated mouse (R. Akagi et al.). Ameliorative effect of deep-sea water on biochemical and mechanical properties of bone in SAMP6 and SAMR1 (Y. Iinuma et al.).
Author index.
Keyword index.
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