Assessment of pathophysiology of detrusor underactivity and sequence of new targets of therapeutic agents
| Project/Area Number |
17H06638
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Urology
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| Research Institution | Jichi Medical University (2018)
The University of Tokyo (2017) |
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Principal Investigator |
Kamei Jun 自治医科大学, 医学部, 講師 (80805622)
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| Project Period (FY) |
2017-08-25 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 排尿機能学 / 加齢医学 / 排尿筋低活動 |
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| Outline of Final Research Achievements |
We tried to establish new detrusor underactivity rat models based on the pathophysiological hypothesis of human detrusor underactivity. Furthermore, we investigated age-related changes in in vitro and in vivo functions and gene expression of the bladder of male and female mice. We evaluated three types of new detrusor underactivity rat models with cystometry or frequency/volume measurements, and found it was very difficult to establish new models of rats with moderate detrusor underactivity with higher reproducibility. In contrast, we found aged mice demonstrated voiding and storage dysfunctions resembling to detrusor hyperactivity with impaired contractility (DHIC), which were more pronounced in male mice. Genomic changes associated with aging may contribute to the age-related bladder functional deterioration in mice.
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| Academic Significance and Societal Importance of the Research Achievements |
さまざまなアプローチ法や条件検討を重ねた結果、病態や薬効評価に適した安定した新規排尿筋低活動モデルラットを作成することは困難であった。一方、今回の研究により、老齢マウスはヒトの膀胱機能の加齢性変化に似た障害を呈することと、膀胱における多数の遺伝子発現が変化していることが判明し、将来的に原因遺伝子の探索に本研究が役立ち、遺伝子改変動物を用いた検討に発展できる可能性が期待できる。
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Report
(3 results)
Research Products
(2 results)
