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Modulation of intestinal gut barrier permeability by dipeptidyl peptidase IV inhibition in a model of rat septicemia / Doaa Abdallah Zaky B.Pharm ; Supervised Dalaal Moustafa Abdallah , Noha Nagah Nassar , Muhammad Yusuf Alshorbagy

By: Contributor(s): Material type: TextTextLanguage: English Publication details: Cairo : Doaa Abdallah Zaky B.Pharm , 2017Description: 158 P. : charts , facsimiles ; 25cmOther title:
  • تعديل نفاذية الحاجز المعوي بتثبيط ثنائي ببتيديل ببتيداز 4 في نموذج لتسمم الدم في الجرذان [Added title page title]
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Dissertation note: Thesis (M.Sc.) - Cairo University - Faculty of Pharmacy- Department of Pharmacology and Toxicology Summary: BThe 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.
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Thesis Thesis قاعة الرسائل الجامعية - الدور الاول المكتبة المركزبة الجديدة - جامعة القاهرة Cai01.08.09.M.Sc.2017.Do.M (Browse shelf(Opens below)) Not for loan 01010110073019000
CD - Rom CD - Rom مخـــزن الرســائل الجـــامعية - البدروم المكتبة المركزبة الجديدة - جامعة القاهرة Cai01.08.09.M.Sc.2017.Do.M (Browse shelf(Opens below)) 73019.CD Not for loan 01020110073019000

Thesis (M.Sc.) - Cairo University - Faculty of Pharmacy- Department of Pharmacology and Toxicology

BThe 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.

Issued also as CD

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