| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥130,000 (Direct Cost: ¥100,000、Indirect Cost: ¥30,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Outline of Final Research Achievements |
This study attempted to further examine the downstream signaling factors in this system by blocking the action of angiotensin II (ATII), hypothesizing that this would lead to similar improvement of intestinal adaptation after SBR. . Because realtime PCR studies showed that only ATII receptor type 1a (ATII-1a) expression was significantly increased after SBR, compared to Sham mice. The apoptotic and proliferation signaling pathways were addressed by analysis of EC. SBR led to a significant increase in villus height and crypt depth. ATII treatment did not significantly change EC proliferation, but did significantly reduce EC apoptosis rates as compared to the nontreated SBR group. This study showed that the ATII-1a receptor may be of crucial importance for the modulation of intestinal EC apoptosis, and for regulating the post-resectional EC adaptive response.
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