000 | 02113cam a2200349 a 4500 | ||
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003 | EG-GiCUC | ||
005 | 20250223031831.0 | ||
008 | 171024s2017 ua dh f m 000 0 eng d | ||
040 |
_aEG-GiCUC _beng _cEG-GiCUC |
||
041 | 0 | _aeng | |
049 | _aDeposite | ||
097 | _aM.Sc | ||
099 | _aCai01.08.09.M.Sc.2017.Do.M | ||
100 | 0 | _aDoaa Abdallah Zaky | |
245 | 1 | 0 |
_aModulation of intestinal gut barrier permeability by dipeptidyl peptidase IV inhibition in a model of rat septicemia / _cDoaa Abdallah Zaky B.Pharm ; Supervised Dalaal Moustafa Abdallah , Noha Nagah Nassar , Muhammad Yusuf Alshorbagy |
246 | 1 | 5 | _aتعديل نفاذية الحاجز المعوي بتثبيط ثنائي ببتيديل ببتيداز 4 في نموذج لتسمم الدم في الجرذان |
260 |
_aCairo : _bDoaa Abdallah Zaky B.Pharm , _c2017 |
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300 |
_a158 P. : _bcharts , facsimiles ; _c25cm |
||
502 | _aThesis (M.Sc.) - Cairo University - Faculty of Pharmacy- Department of Pharmacology and Toxicology | ||
520 | _aBThe preferential role of the underlying PI3K/Akt (PKB) axis in triggering enterocytic proliferation/differentiation signaling and AJ assembly is still controversial. The involvement of CD26/DPP-IV in obstructive jaundice (OJ)-induced sepsis has not been yet reported VLD3/10/30 dose dependently modulated CD26/DPP-IV, GLP-1, IGF-1, PI3K, pS473-Akt, pS9-GSK-3Ý, pS133-CREB, and CD1. VLD3/10 increased E-cadherin and NPSH, however, they reduced pY654-Ý-catenin, portal and aortic endotoxin, NF-mB, TNF-Ü, MPO, TBARS, subepithelial/pericryptal and submucosal collagen deposition as well as vimentin immunoreactivity, effects that were quite opposed with VLD30. | ||
530 | _aIssued also as CD | ||
653 | 4 | _aAdherens junctions | |
653 | 4 | _aOxidative stress | |
653 | 4 | _aVildagliptin | |
700 | 0 |
_aDalaal Moustafa Abdallah , _eSupervisor |
|
700 | 0 |
_aMuhammad Yusuf Alshorbagy , _eSupervisor |
|
700 | 0 |
_aNoha Nagah Nassar , _eSupervisor |
|
856 | _uhttp://172.23.153.220/th.pdf | ||
905 |
_aNazla _eRevisor |
||
905 |
_aShimaa _eCataloger |
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942 |
_2ddc _cTH |
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999 |
_c63119 _d63119 |