| Project/Area Number |
60570877
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Functional basic dentistry
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| Research Institution | Josai Dental University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KASHIMATA Masanori 城西歯科大学, 歯学部, 助手 (30152630)
MINAMI Naomi 城西歯科大学, 歯学部, 教授 (20049349)
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| Project Period (FY) |
1985 – 1986
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| Project Status |
Completed (Fiscal Year 1986)
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| Budget Amount *help |
¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1986: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1985: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | Epidermal growth factor (EGF) / Enzyme immunoassay / Salivary gland / Kidney / Small intestine / EGF receptor / 実験的糖尿病 |
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| Research Abstract |
1. We developed an enzyme immunoassay for epidermal growth factor (EGF) in a liquid phase double antibody system. This method can detect as low as 20 pg EGF per tube, and the sensitivity seems to be equal or rather higher than that of radioimmunoassay or radioreceptor assay.
2. In addition to the submandibular gland, EGF was detected in various tissues of mice. As is the case of the submandibular gland, a marked sex difference in EGF concentration was found in the sublingual and parotid glands.
3. The molecular weight of EGF in the sublingual gland and kidney was the same as that of EGF in the submandibular gland. The isoelectric points of EGF in these tissues were between pH 4.3 and 4.6. By reverse-phase HPLC, two forms of EGF ( <alpha> -EGF and <beta> -EGF) were detected in the kidney and sublingual gland preparations.
4. The extirpation of submandibular gland significantly decreased protein, DNA and RNA concentrations in the duodenum and jejunum of adult mice. These decreases were restored to normal levels by the administration of EGF. From these results, it is suggested that EGF in the submandibular gland acts as a trophic factor for the small intestine.
5. The effect of streptozotocin-induced diabetes on <^(125)I> -labeled EGF binding was studied in microsomal membranes from the rat liver. The binding of EGF in membranes from diabetic animals was found to be significantly low. Scatchard analysis of the binding data clearly showed that the decrease in EGF binding was due to a decrease in the number of receptors. Treatment of diabetic animals with insulin restored EGF receptor numbers to control levels. These results suggest that insulin deficiency in vivo causes a decrease in hepatic EGF receptors.
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