| Co-Investigator(Kenkyū-buntansha) |
ASAI Shyuuichi Japan S.L.C.(Co.), Principal Investigator, 研究員
AWAT Takuya Saitama Medical School, 4th dept. Internal Medicine, Medicine, Assistant Professor, 医学部, 助教授 (40184303)
KOMEDA Kjyurou Tokyo Medical University, Animal Research Center, Medicine, Professor, 医学部, 教授 (90074533)
KAWAMOTO Eiichi Tokyo Medical University, Animal Research Center, Medicine, Assistant Professor, 医学部, 講師 (20074718)
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| Research Abstract |
The RT1 class II area is u/u in BB/W rats, insulitis occurs, resulting type 1 DM. When the area is a/a, thyoiditis occurs, resulting in Hashimoto's disease.
In the present study, a large number of rats developing Hashimoto's disease and rats with hereditary stability were prepared. The following rats were prepared in the present study:
Type u/u: 82 males and 76 females, totaling 158 rats.
Type u/a: 94 males and 111 females, totaling 205 rats.
Type a/a: 28 males and 32 females, totaling 60 rats.
There were 423 rats in total.
Hereditary stabilization was induced by repeated back-crossing. In the 10th generation, all chromosomes other than chromosome No.20 were fixed to a homogeneous genotype. Chromosome No.20, which includes the area of the major histocompatibility complex (MHC), still showed a heterogeneous genotype.
The type a/a rats developed thuroiditis at an incidence of approximately 90% about 210 days after the preparation. The blood level of thyroid hormones were low in these rats, but the pathological findings of thyroiditis were not completely consistent with the blood level of the thyroid hormones.
In the future, a stable supply of thyroiditis model rats, by the development of rats with fixation of chromosome No.20 as well to the homogeneous genotype, will become increasingly necessary.
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