Bone disorder in cardiomyopathic hamsters

Togari, Akifumi; Arai, Michitsugu; Matsumoto, Shosei; Tarumoto, Yasuo; Takahashi, Hisahide

doi:10.1016/0169-6009(89)90070-6

Bone and Mineral

1989

DOI: 10.1016/0169-6009(89)90070-6

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Bone disorder in cardiomyopathic hamsters

Akifumi Togari¹,

Michitsugu Arai²,

Shosei Matsumoto³

et al.

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1991

2001

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Cited by 4 publications

(3 citation statements)

References 18 publications

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“…The UM-X7.1 syrian hamsters is known as one of the animal models for idiopathic cardiomyopathy and congestive heart failure (Bajusz, 1969;Homburger, 1979;Factor, 1982;Makino, 1985). Moreover, the UM-X7.1 syrian hamsters demonstrates a high level of plasma calcium and bone disorder (Togari, 1989). Previously, we reported that in the UM-X7.1 syrian hamster, the functional activity of the parathyroid gland may be higher than that of the normal hamster ultrastructurally (Utsumi, 1999).…”

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confidence: 99%

Histopatholoeic Features of Masseter Muscle in the Distrophic Hamster (UM-X7. 1 Syrian Hamster)

Mizutani

Utsumi

Moriguchi

et al. 2001

Okajimas Folia Anatomica Japonica

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Summary: Dystrophic hamster has been regarded as the useful model animal for Severe childhood autosomal recessive muscular dystrophy (SCARMD). Although, many studies on Dystrophic hamster have utilized the muscular tissue of the trunk, however no study have been analyzed for the masticatory muscle. For this study, we used a Dystrophic hamster (UM-X7.1 Syrian hamster) to histochemically investigate the effect of muscular dystrophy on the masseter muscle. Large and small regenerated muscle fibers, and necrotic fibers were detected almost in all areas. Opaque fiber, hypertrophic fiber with fiber splitting structure and necrotic fiber filled up by mononuclear phagocytes were recognized. The region, in which the mononuclear phagocytic cells infiltrated, showed strong positivity to acid phosphatase, and lysosome enzyme. There were many muscle fibers with reduced levels of succinate dehydrogenase (SDH) activities in the muscle fiber. Some TUNEL-positive cells were confirmed in both necrotic and non-necrotic areas. It was suggested that a part of TUNEL-positive cells are the cells originated from the connective tissue or immunocytes. In this result, histopathologic changes of the masseter muscle of the UM-X7.1 Syrian hamster was similar to muscle of the body trunk in the past reports. As the result, it was suggested that jaw closing movements may be negatively affected caused by the decline of the masseter muscle twitch. And, the point of view by which apoptosis is the trigger for the muscle fiber collapse were not seen in the Dystrophic hamster masseter muscle. We suggest that apoptosis is a one step in the process of regeneration of muscle fibers.

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mentioning

confidence: 99%

Histopatholoeic Features of Masseter Muscle in the Distrophic Hamster (UM-X7. 1 Syrian Hamster)

Mizutani

Utsumi

Moriguchi

et al. 2001

Okajimas Folia Anatomica Japonica

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“…Right tibiae were defatted, dried and reduced to ashes according to the procedure described in our previous study (13). The ash was dissolved in 6 N HC1, and calcium and phosphorus concentrations were determined in the same way as those in the plasma.…”

mentioning

confidence: 99%

“…The ash was dissolved in 6 N HC1, and calcium and phosphorus concentrations were determined in the same way as those in the plasma. From the left tibiae and femora, undecalcified frontal sections of proximal tibiae and transverse sections of the femora at the mid-point, all 50-pm-thick, were prepared (13). Fluorescent micrographs and contact microradiographs (CMR) of the ground sections were taken with a fluorescence microscope and a soft X-ray apparatus (Sofron, Soken Co., Tokyo), respectively.…”

mentioning

confidence: 99%

Alteration of Bone Status with Ascorbic Acid Deficiency in ODS (Osteogenic Disorder Shionogi) Rats

Togari

Arai

Nakagawa

et al. 1995

Japanese Journal of Pharmacology

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ABSTRACT-Ratswith hereditary defects in ascorbic acid (AsA) synthesis (ODS rats) subjected to AsAdeficiency for 3 weeks showed reductions of plasma alkaline phosphatase and dry and ash weights of the tibia, but no body weight alteration. In accordance with the chemical changes, bone loss and decrease of bone formation by AsA deficiency but not by malnutrition were observed in contact microradiographs of the tibia and by a tetracycline double labeling technique, respectively. The mechanical properties of femora measured by a three point-bending procedure were also altered by AsA deficiency for 3 weeks and showed decreases of 59% in toughness, 32% in strength, 32% in ductility and 22% in stiffness. The biomechanical changes by AsA deficiency were greater than the chemical changes in bone, indicating the usefulness of measuring mechanical properties as a sensitive method for the evaluation of the bone status. The second moment of the area of the femur was not changed by AsA deficiency. These results suggest that AsA deficiency in ODS rats causes marked bone loss and reduction in bone formation, which is accompanied by a greater reduction in biomechanics of the femur without causing macroarchitectural changes.

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Fluid movement in bone: Theoretical and empirical

Dillaman

Roer

Gay

1991

Journal of Biomechanics

132

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Bone disorder in cardiomyopathic hamsters

Cited by 4 publications

References 18 publications

Histopatholoeic Features of Masseter Muscle in the Distrophic Hamster (UM-X7. 1 Syrian Hamster)

Histopatholoeic Features of Masseter Muscle in the Distrophic Hamster (UM-X7. 1 Syrian Hamster)

Alteration of Bone Status with Ascorbic Acid Deficiency in ODS (Osteogenic Disorder Shionogi) Rats

Fluid movement in bone: Theoretical and empirical

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