The Experts below are selected from a list of 3267 Experts worldwide ranked by ideXlab platform
Keiichi Higuchi - One of the best experts on this subject based on the ideXlab platform.
-
The Senescence-Accelerated Mouse as a model for geriatrics and aging biology
Nihon yakurigaku zasshi. Folia pharmacologica Japonica, 2019Co-Authors: Masayuki Mori, Keiichi HiguchiAbstract:Rapid expansion of aged population is predicted worldwide. To cope with problems expected from this situation and extend the period of active and healthy life of people as much as possible, it is important to elucidate not only the biological mechanisms of "aging", but also the etiology of various "age-related diseases". To attain this goal, extensive studies using excellent animal models are indispensable. Senescence-Accelerated Mouse (SAM) is a series of inbred Mouse strains that includes SAMP1, SAMP6, SAMP8, SAMP10, and SAMR1. SAMP strains exhibit Accelerated Senescence and short lifespan. In addition, each strain shows specific age-related disease phenotypes which are similar to symptoms observed in humans, such as senile amyloidosis (SAMP1), senile osteoporosis (SAMP6), and age-dependent deficits in learning and memory (SAMP8), making SAM mice useful for an aging research. In this review, we introduce the characteristics and application of SAM in geriatrics and aging biology.
-
Senescence-Accelerated Mouse (SAM) strains have a spontaneous mutation in the Abcb1a gene.
Experimental animals, 2008Co-Authors: Guohong Zhang, Keiichi Higuchi, Beiru Zhang, Hiroshi Tomozawa, Kiyoshi Matsumoto, Masayuki MoriAbstract:Senescence-Accelerated Mouse (SAM) strains are used as animal models for gerontological research. Here, we report that the SAMR1 strain, which shows a high sensitivity to toxicity of the parasiticide ivermectin, has a spontaneous retroviral insertional mutation in the ATP-binding cassette, sub-family B (MDR/TAP), member 1A (Abcb1a) gene. This mutation is identical to that found in Crl:CF1-Abcb1a mice, which are also highly sensitive to ivermectin due to the mutation. The mutant Abcb1a allele was found in SAMR4, SAMR5, SAMP1, SAMP6, SAMP7, and SAMP9, but not in SAMP3, SAMP8, SAMP10, SAMP11, and other outbred and inbred strains, including 129/SvJ strains. These results impart both caution and promise in the use of SAM strains in studies of biological processes in which P-glycoprotein participates.
-
Identification of differentially expressed genes in Senescence-Accelerated Mouse testes by suppression subtractive hybridization analysis
Mammalian Genome, 2007Co-Authors: Takuya Chiba, Masanori Hosokawa, Yoshikazu Higami, Isao Shimokawa, Keiichi HiguchiAbstract:Senescence-Accelerated Mouse (SAM) strains constitute a model of Accelerated Senescence coupled with a short lifespan and the early development of various age-related disorders. To identify differential gene expression in testes between Senescence-Accelerated SAMP1 and control SAMR1 mice, we performed suppression subtractive hybridization. We observed that the expression of three genes related to cell proliferation (myosin regulatory light chain B, aldolase 1A isoform, and cytochrome c oxidase subunit VIc) were upregulated and four genes implicated in spermatogenesis were downregulated in SAMP1 mice. Asb-8, a member of ankyrin repeat-containing proteins, was abundantly expressed in the testes and downregulated in SAMP1. The other three downregulated genes (germ cell-specific gene 1, T-complex polypeptide 1b, and activator of cAMP responsive element modulator in testis) have been reported to regulate late-stage spermatogenesis. These gene expression profiles might explain the findings of early testicular maturation and rapid decline in the ability to produce spermatozoa with advancing age in SAMP1 mice.
-
Dietary fat modulation of apoA-II metabolism and prevention of senile amyloidosis in the Senescence- Accelerated Mouse.
Journal of lipid research, 2003Co-Authors: Makiko Umezawa, Masanori Hosokawa, Toshio Takeda, Kenjiro Tatematsu, Tatsumi Korenaga, Takatoshi Matushita, Harumi Okuyama, Keiichi HiguchiAbstract:Senescence-Accelerated Mouse-prone (SAMP1; SAMP1@Umz) is an animal model of senile amyloidosis with apolipoprotein A-II (apoA-II) amyloid fibril (AApoAII) deposits. This study was undertaken to investigate the effects of dietary fats on AApoAII deposits in SAMP1 mice when purified diets containing 4% fat as butter, safflower oil, or fish oil were fed to male mice for 26 weeks. The serum HDL cholesterol was significantly lower (P butter > safflower oil group, P < 0.05). These findings suggest that dietary fats differ in their effects on serum lipoprotein metabolism, and that dietary lipids may modulate amyloid deposition in SAMP1 mice.-Umezawa, M., K. Tatematsu, T.
-
Unique Mutations in Mitochondrial DNA of Senescence-Accelerated Mouse (SAM) Strains
The Journal of heredity, 2001Co-Authors: J. Mizutani, Keiichi Higuchi, Takuya Chiba, Masashi Tanaka, Masayuki MoriAbstract:Mitochondrial DNA (mtDNA) is exclusively inherited maternally and hence could offer a good method for tracing the lineage of Mouse strains. We examined the mtDNA sequence of Senescence-Accelerated Mouse (SAM) strains as well as other laboratory strains of inbred mice to deduce the ancestral strain of SAM. Four unique mutations were identified at bases 2256, 10,847, 11,181, and 13,053 in SAM strains. The mutations were not found in other Mouse strains including AKR/J, one of the parental strains of SAM. Comparison of the mtDNA sequences also led to the consensus mtDNA sequence of laboratory strains of inbred mice. The seven laboratory strains of common inbred mice showed polymorphisms at base 9348, thymine repeat from base 9818, and adenine repeat from base 9821, and could be classified into five types by combination of the differences. Although we could not identify Mouse strains with the same type of mtDNA as SAM in this study, the polymorphisms would provide a promising clue to ascertain the ancestral strain(s) of SAM. The polymorphism in mtDNA could be used to ascertain the genealogy of other Mouse strains as well.
Masanori Hosokawa - One of the best experts on this subject based on the ideXlab platform.
-
Identification of differentially expressed genes in Senescence-Accelerated Mouse testes by suppression subtractive hybridization analysis
Mammalian Genome, 2007Co-Authors: Takuya Chiba, Masanori Hosokawa, Yoshikazu Higami, Isao Shimokawa, Keiichi HiguchiAbstract:Senescence-Accelerated Mouse (SAM) strains constitute a model of Accelerated Senescence coupled with a short lifespan and the early development of various age-related disorders. To identify differential gene expression in testes between Senescence-Accelerated SAMP1 and control SAMR1 mice, we performed suppression subtractive hybridization. We observed that the expression of three genes related to cell proliferation (myosin regulatory light chain B, aldolase 1A isoform, and cytochrome c oxidase subunit VIc) were upregulated and four genes implicated in spermatogenesis were downregulated in SAMP1 mice. Asb-8, a member of ankyrin repeat-containing proteins, was abundantly expressed in the testes and downregulated in SAMP1. The other three downregulated genes (germ cell-specific gene 1, T-complex polypeptide 1b, and activator of cAMP responsive element modulator in testis) have been reported to regulate late-stage spermatogenesis. These gene expression profiles might explain the findings of early testicular maturation and rapid decline in the ability to produce spermatozoa with advancing age in SAMP1 mice.
-
Dietary fat modulation of apoA-II metabolism and prevention of senile amyloidosis in the Senescence- Accelerated Mouse.
Journal of lipid research, 2003Co-Authors: Makiko Umezawa, Masanori Hosokawa, Toshio Takeda, Kenjiro Tatematsu, Tatsumi Korenaga, Takatoshi Matushita, Harumi Okuyama, Keiichi HiguchiAbstract:Senescence-Accelerated Mouse-prone (SAMP1; SAMP1@Umz) is an animal model of senile amyloidosis with apolipoprotein A-II (apoA-II) amyloid fibril (AApoAII) deposits. This study was undertaken to investigate the effects of dietary fats on AApoAII deposits in SAMP1 mice when purified diets containing 4% fat as butter, safflower oil, or fish oil were fed to male mice for 26 weeks. The serum HDL cholesterol was significantly lower (P butter > safflower oil group, P < 0.05). These findings suggest that dietary fats differ in their effects on serum lipoprotein metabolism, and that dietary lipids may modulate amyloid deposition in SAMP1 mice.-Umezawa, M., K. Tatematsu, T.
-
Tubular aggregates in the skeletal muscle of the Senescence-Accelerated Mouse; SAM.
Mechanisms of ageing and development, 2000Co-Authors: Tomofumi Nishikawa, Keiichi Higuchi, Jun A. Takahashi, Takatoshi Matsushita, Katsunori Ohnishi, Nobuo Hashimoto, Masanori HosokawaAbstract:We investigated the skeletal muscles of nine strains of Senescence Accelerated Mouse (SAM), DDD, AKR/J, C57BL/6J, A/J and BALB/c mice. We found that male SAMP8, SAMP7, C57BL/6J, A/J and BALB/c mice expressed tubular aggregates (TAs) in their skeletal muscle. Among these strains, the SAMP8 strain, which exhibits a short life span and various age-associated neurodegenerative disorders plus mitochondrial dysfunction, showed TAs more markedly than the others. Thus, we compared SAMP8 mice against SAMR1 mice, an Accelerated Senescence-resistant strain. Light- and electron micrographs showed that male SAMP8 mice exhibited an age-dependent aggravation of TA accumulation. There were no significant differences in the serum lactate/pyruvate levels between the SAMP8 and SAMR1 mice. However, the serum creatine kinase (CK) levels of the 3 and 6-month-old SAMP8 mice were higher than that of the corresponding SAMR1 mice. Considering the serum CK levels and the mitochondrial dysfunction of SAMP8 mice, we conclude that the TAs may be involved in the homeostasis of energy metabolism that is not appropriately regulated in the SAMP8 Mouse mitochondrion.
-
Genetic typing of the Senescence-Accelerated Mouse (SAM) strains with microsatellite markers.
Mammalian genome : official journal of the International Mammalian Genome Society, 1999Co-Authors: Chen Xia, Keiichi Higuchi, Takuya Chiba, Takatoshi Matsushita, Motoyuki Shimizu, Kumiko Kogishi, Jing Wang, Michael F. W. Festing, Masanori HosokawaAbstract:The Senescence-Accelerated Mouse (SAM) strains constitute a murine model of Accelerated Senescence originating from the ancestral AKR/J strains and consist of nine Senescence-prone (SAMP) strains and four Senescence-resistant (SAMR) strains. The chromosomes (Chrs) of the SAM strains were typed with 581 microsatellite markers amplified by PCR, and the fundamental genetic information of the SAM strains was obtained. One-third of the examined markers displayed polymorphism among the strains, and only two alleles were detected in almost all loci among the SAM and AKR/J strains. However, in 12 loci (5.6% of total 215 polymorphic markers), the third allele was detected among the SAM strains. The genetic typing and developmental history suggested that the SAM strains were related inbred strains developed by the accidental crossing between the AKR/J strain and other unknown strain(s). Comparison of the distribution of the loci in the SAMP and the SAMR series revealed notable differences in the four regions on Chrs 4, 14, 16, and 17. This indicated that some of these chromosomal sites might contain the genes responsible for Accelerated Senescence in the SAMP series.
-
Senescence-Accelerated Mouse.
Methods in enzymology, 1999Co-Authors: Keiichi Higuchi, Masanori Hosokawa, Toshio TakedaAbstract:Publisher Summary Success has been achieved in developing Senescence-prone inbred strains (SAMP) with Accelerated Senescence and age-associated pathologies and also Senescence-resistant inbred strains (SAMR) with normal aging except for manifestation of nonthymic lymphomas and histiocytic sarcoma. Advances in biomedical research depend to a considerable extent on the availability of relevant and appropriate animal models, particularly animals that have not been subjected to experimental manipulation. This is especially true for a model of aging in which aging progresses insidiously and irreversibly without apparent causes. This is the case with the SAM model in which selective breeding is the only manipulation. This chapter describes a brief history of Senescence-Accelerated Mouse (SAM) development, aging characteristics, pathobiological phenotypes, genetic background, and amyloidosis. Characteristic features of aging in the SAM model were analyzed based on data from the following parameters: (1) growth curve, (2) grading score of Senescence, (3) survivorship curve, (4) Gompertz function, and (5) life span.
Toshio Takeda - One of the best experts on this subject based on the ideXlab platform.
-
Dietary fat modulation of apoA-II metabolism and prevention of senile amyloidosis in the Senescence- Accelerated Mouse.
Journal of lipid research, 2003Co-Authors: Makiko Umezawa, Masanori Hosokawa, Toshio Takeda, Kenjiro Tatematsu, Tatsumi Korenaga, Takatoshi Matushita, Harumi Okuyama, Keiichi HiguchiAbstract:Senescence-Accelerated Mouse-prone (SAMP1; SAMP1@Umz) is an animal model of senile amyloidosis with apolipoprotein A-II (apoA-II) amyloid fibril (AApoAII) deposits. This study was undertaken to investigate the effects of dietary fats on AApoAII deposits in SAMP1 mice when purified diets containing 4% fat as butter, safflower oil, or fish oil were fed to male mice for 26 weeks. The serum HDL cholesterol was significantly lower (P butter > safflower oil group, P < 0.05). These findings suggest that dietary fats differ in their effects on serum lipoprotein metabolism, and that dietary lipids may modulate amyloid deposition in SAMP1 mice.-Umezawa, M., K. Tatematsu, T.
-
Senescence-Accelerated Mouse.
Methods in enzymology, 1999Co-Authors: Keiichi Higuchi, Masanori Hosokawa, Toshio TakedaAbstract:Publisher Summary Success has been achieved in developing Senescence-prone inbred strains (SAMP) with Accelerated Senescence and age-associated pathologies and also Senescence-resistant inbred strains (SAMR) with normal aging except for manifestation of nonthymic lymphomas and histiocytic sarcoma. Advances in biomedical research depend to a considerable extent on the availability of relevant and appropriate animal models, particularly animals that have not been subjected to experimental manipulation. This is especially true for a model of aging in which aging progresses insidiously and irreversibly without apparent causes. This is the case with the SAM model in which selective breeding is the only manipulation. This chapter describes a brief history of Senescence-Accelerated Mouse (SAM) development, aging characteristics, pathobiological phenotypes, genetic background, and amyloidosis. Characteristic features of aging in the SAM model were analyzed based on data from the following parameters: (1) growth curve, (2) grading score of Senescence, (3) survivorship curve, (4) Gompertz function, and (5) life span.
-
Senescence-Accelerated Mouse (SAM): a biogerontological resource in aging research.
Neurobiology of aging, 1999Co-Authors: Toshio TakedaAbstract:The Senescence-Accelerated Mouse (SAM), consisting of 14 Senescence-prone inbred strains (SAMP) and 4 Senescence-resistant inbred strains (SAMR) has been under development since 1970 through the selective inbreeding of AKR/J strain mice donated by the Jackson laboratory in 1968, based on the data of the grading score of Senescence, life span, and pathologic phenotypes. The characteristic feature of aging common to all SAMP and SAMR mice is Accelerated Senescence and normal aging, respectively. Furthermore, SAMP and SAMR strains manifest various pathobiological phenotypes which include such neurobiological phenotypes as deficits in learning and memory, emotional disorders, abnormal circadian rhythms, brain atrophy, hearing impairment, etc., and are often characteristic enough to differentiate the strains. Various efforts are currently being made using the SAM model to clarify the underlying mechanisms in Accelerated Senescence as well as the etiopathogenic mechanisms in age-associated pathobiologies. Genetic background and significance of SAM development are discussed.
-
A novel murine model of aging, Senescence-Accelerated Mouse (SAM)
Archives of gerontology and geriatrics, 1994Co-Authors: Toshio Takeda, Keiichi Higuchi, Masanori Hosokawa, Masamichi Hosono, Ichiro Akiguchi, Hideki KatohAbstract:Senescence-Accelerated Mouse (SAM) has been under development by our research team at Kyoto University since 1970, based on the AKR/J strain donated by the Jackson Laboratory in 1968. The SAM Mouse has an Accelerated Senescence and age-associated pathologies such as senile amyloidosis, senile osteoporosis, degenerative joint disease, cataract, deficits in learning and memory, brain atrophy, hyperinflation of lungs, hearing impairment and so on. SAM research is advancing world-wide and attempts are being made to clarify fundamental mechanisms involved in primary aging processes, pathogenesis of age-associated pathologies and effective methods to modulate or ameliorate the advance of Senescence and disease processes involved in age-associated pathologies.
-
Beta/A4 proteinlike immunoreactive granular structures in the brain of Senescence-Accelerated Mouse.
The American journal of pathology, 1993Co-Authors: Manabu Takemura, S. Ishikawa, Ichiro Akiguchi, S. Nakamura, Masaki Ueno, N. Oka, A. Shimada, Jun Kimura, Toshio TakedaAbstract:The immunohistochemical localization of amyloid beta/A4 protein in the Senescence-Accelerated Mouse brain was studied using six different antisera against human amyloid precursor protein peptides. beta/A4 proteinlike immunoreactivity was observed in the form of granular structures (beta-LIGS) in various regions, including the medial septum, cerebral cortex, hippocampus, cerebellum, and some cranial nerve roots. beta-LIGS were 1.5 to 2.5 mu in diameter and irregularly shaped. They increased significantly in number with aging, predominantly in animals with a phenotype of age-related deterioration of memory and learning abilities. Congo red and thioflavine S did not stain the granules. On immunoblots, the main immunoreactive bands were observed at 14 to 18 kd. The staining intensities of these bands also increased with advancing age. We consider that beta-LIGS are not only a new morphological manifestation of Senescence in mice, but also a pertinent clue in understanding the mechanisms of amyloid deposition.
Yoshinosuke Fukuchi - One of the best experts on this subject based on the ideXlab platform.
-
Tomato juice prevents Senescence-Accelerated Mouse P1 strain from developing emphysema induced by chronic exposure to tobacco smoke.
American journal of physiology. Lung cellular and molecular physiology, 2005Co-Authors: Satoshi Kasagi, Kuniaki Seyama, Hiroaki Mori, Sanae Souma, Tadashi Sato, Taeko Akiyoshi, Hiroyuki Suganuma, Yoshinosuke FukuchiAbstract:The Senescence-Accelerated Mouse (SAM) is a naturally occurring animal model for Accelerated aging after normal development and maturation. SAMP1 strain was reported to show age-related structural ...
-
Biochemical characteristics of lungs in Senescence-Accelerated Mouse (SAM)
The European respiratory journal, 1995Co-Authors: Shinji Teramoto, Yoshinosuke Fukuchi, Yasuhide Uejima, Kazuko Teramoto, H OrimoAbstract:This study examined age-related biochemical changes of the lung in an animal model of senile lung, Senescence-Accelerated Mouse (SAM). Bronchoalveolar lavage (BAL) was performed on two strains of SAM, the Senescence-prone strain (SAM P2) and the Senescence-resistant strain (SAM R1), as well as on normal ageing C57 black mice (C57BL), aged 1-24 months. Elastase-like and elastase inhibitory activity of BAL fluid (BALF), glutathione (GSH) and oxidized GSH (GSSG) content both of BALF and lung tissue, and oxygen radical generation of free lung cells obtained by BAL were examined in the three strains of mice. Cell populations did not change throughout the life in SAM strains and C57BL. The elastolytic activity in SAM was greater than in C57BL, but there was no change with age. Both a decreased content of GSH and an increased oxidation of the GSH in BALF were markedly observed with ageing in SAM P2. In the lung tissue, the GSSG/GSH ratio in SAM strains was consistently greater than that in C57BL, suggesting that the GSH redox cycle of the lung may be impaired in SAM strains. The oxygen radical generation by free lung cells increased with age in all three strains, but the increase was earlier and more pronounced in SAM P2 than in the other two strains. In conclusion, an impaired GSH redox cycle and an increased formation of oxygen radicals are observed in the lungs of SAM with increasing age.
-
A novel model of senile lung: Senescence-Accelerated Mouse (SAM).
American journal of respiratory and critical care medicine, 1994Co-Authors: Shinji Teramoto, Yoshinosuke Fukuchi, Yasuhide Uejima, Kazuko Teramoto, Teruaki Oka, Hajime OrimoAbstract:Senescence-Accelerated Mouse (SAM) has been characterized as a unique animal model to investigate spontaneous aging as well as age-related disorders. However, little is known about the properties of the lung. We examined age-related morphologic and functional changes of the lung in SAM P2, as the Senescence-prone strain, and in SAM R1, as the Senescence-resistant strain. On morphologic examination, the earlier (starting at 6 mo) and more severe change in airspace size (mean linear intercept: MLI) was observed in SAM P2 (MLI [micron]; 3 mo: 72.1 +/- 2.4; 6 mo: 80.8 +/- 2.9; 12 mo: 91.1 +/- 3.1; 18 mo: 143.4 +/- 6.6), compared with SAM R1 (MLI [micron]; 3 mo: 68.9 +/- 1.8; 6 mo: 70.8 +/- 2.6; 12 mo: 76.1 +/- 2.8; 18 mo: 101.2 +/- 4.7). The destructive index was not remarkably changed through life in both strains, suggesting that the alveolar wall was relatively intact in SAM. On functional examination, the left-sided shift of the pressure-volume (P-V) curves observed in SAM P2 at an early stage of aging (st...
Yoshinori Umesaki - One of the best experts on this subject based on the ideXlab platform.
-
Inflammatory bowel disease-like enteritis and caecitis in a Senescence Accelerated Mouse P1/Yit strain
Gut, 1998Co-Authors: Satoshi Matsumoto, Okabe Y, Hiromi Setoyama, K Takayama, J Ohtsuka, Funahashi H, Akemi Imaoka, Okada Y, Yoshinori UmesakiAbstract:Background—A new subline of the Senescence Accelerated Mouse (SAM) P1/Yit strain has been established which shows spontaneous enteric inflammation under specific pathogen free (SPF) conditions. Aims—To elucidate the pathogenesis of enteric inflammation in this new subline. Methods—The SPF and germ free (GF) SAMP1/Yit strains were used. Histological, immunological, and microbiological characterisation of the mice with enteric inflammation was performed. Results—Histologically, enteritic inflammation developed as a discontinuous lesion in the terminal ileum and caecum with the infiltration of many inflammatory cells after 10 weeks of age. The activity of myeloperoxidase, and both immunolocalisation and mRNA expression of inducible nitric oxide synthase increased in the lesion. CD3-e positive T cells, neutrophils, and macrophages were more numerous in the inflamed mucosa of the SAMP1/Yit strain. The GF SAMP1/Yit strain did not show any inflammation in the intestinal wall, by the age of 30 weeks, and the enteritis and caecitis developed 10 weeks after the conventionalisation of the GF SAMP1/Yit strain. Conclusion—Enteric inflammation in the ileum and caecum developed in the SAMP1/Yit strain. The pathophysiological characteristics of the disease in this Mouse have some similarities to those of human inflammatory bowel disease (IBD). This Mouse strain should be a useful model system for elucidating the interaction between the pathogenesis of IBD and the gut microflora. Keywords: inflammatory bowel disease; enteritis; caecitis; Senescence Accelerated Mouse
-
inflammatory bowel disease like enteritis and caecitis in a Senescence Accelerated Mouse p1 yit strain
Gut, 1998Co-Authors: Satoshi Matsumoto, Hiromi Setoyama, K Takayama, J Ohtsuka, Akemi Imaoka, Y Okabe, H Funahashi, Y Okada, Yoshinori UmesakiAbstract:Background—A new subline of the Senescence Accelerated Mouse (SAM) P1/Yit strain has been established which shows spontaneous enteric inflammation under specific pathogen free (SPF) conditions. Aims—To elucidate the pathogenesis of enteric inflammation in this new subline. Methods—The SPF and germ free (GF) SAMP1/Yit strains were used. Histological, immunological, and microbiological characterisation of the mice with enteric inflammation was performed. Results—Histologically, enteritic inflammation developed as a discontinuous lesion in the terminal ileum and caecum with the infiltration of many inflammatory cells after 10 weeks of age. The activity of myeloperoxidase, and both immunolocalisation and mRNA expression of inducible nitric oxide synthase increased in the lesion. CD3-e positive T cells, neutrophils, and macrophages were more numerous in the inflamed mucosa of the SAMP1/Yit strain. The GF SAMP1/Yit strain did not show any inflammation in the intestinal wall, by the age of 30 weeks, and the enteritis and caecitis developed 10 weeks after the conventionalisation of the GF SAMP1/Yit strain. Conclusion—Enteric inflammation in the ileum and caecum developed in the SAMP1/Yit strain. The pathophysiological characteristics of the disease in this Mouse have some similarities to those of human inflammatory bowel disease (IBD). This Mouse strain should be a useful model system for elucidating the interaction between the pathogenesis of IBD and the gut microflora. Keywords: inflammatory bowel disease; enteritis; caecitis; Senescence Accelerated Mouse
