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Attalla, D. M., L. A. Ahmed, H. F. Zaki, and M. M. Khattab, "Paradoxical effects of atorvastatin in isoproterenol-induced cardiotoxicity in rats: role of oxidative stress and inflammation", Biomedicine & Pharmacotherapy, vol. 104: Elsevier Masson, pp. 542–549, 2018. Abstract
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NO, R., A. LA, A. DM, and E. - S. BM, "Paradoxical cardiotoxicity of intraperitoneally-injected epigallocatechin gallate preparation in diabetic mice.", Sci Rep. , vol. 8, issue 1, pp. 7880, 2018.
Rasheed, N. A. O., L. A. Ahmed, D. M. Abdallah, and B. M. El-Sayeh, "Paradoxical cardiotoxicity of intraperitoneally-injected epigallocatechin gallate preparation in diabetic mice", Scientific reports, vol. 8, pp. 7880, 1979 Oct, 2018. Abstract

It has been found that NADPH-dependent hydroxylation of dimethylaniline, aniline, p- and o-nitroanisol and lipid peroxidation is inhibited by the tyrosine-copper (II) complex (low molecular weight analog of superoxide dismutase), which is indicative of a possibility of superoxide radicals formation in these reactions. The inhibition of the above-mentioned reactions with Tyr2-Cu2+ is less pronounced or absent, if cumole hydroperoxide is used as cosubstrate instead of NADPH. Differences in the Tyr2-Cu2+ complex effects on the cumule hydroperoxide-dependent xenobiotics hydroxylation and lipid peroxidation catalyzed by various forms of cytochrome P-450, e. g. microsomal, soluble and incorporated into liposomes, have been found. The data obtained suggest that the efficiency of the inhibitory effect of the Tyr2-Cu2+ complex depends on the type of cosubstrates (NADPH, cumole hydroperoxide) and substrates used as well as on the form of cytochrome P-450.

Rasheed, N. A. O., L. A. Ahmed, D. M. Abdallah, and B. M. El-Sayeh, "Paradoxical cardiotoxicity of intraperitoneally-injected epigallocatechin gallate preparation in diabetic mice", Scientific Reports, vol. 8, no. 1: Nature Publishing Group UK London, pp. 7880, 2018. Abstract
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Zaky, D. A., D. M. Abouelfadl, N. N. Nassar, D. M. Abdallah, and M. Y. Al-Shorbagy, "The paradox of dipeptidyl peptidase IV inhibition in enterocytic differentiation and epithelial-mesenchymal transition in rat cholestatic sepsis.", Toxicology and applied pharmacology, vol. 394, pp. 114956, 2020. Abstract

Proper enterocytic proliferation/differentiation, besides providing adequate adherens junctions (AJ) integrity, are responsible for strengthening of the gut barrier that acts as a first line defense against endotoxemia. However, the preferential role of the underlying PI3K/Akt (PKB) axis in triggering enterocytic proliferation/differentiation signaling and AJ assembly is still obscure in sepsis. Additionally, the potential involvement of dipeptidyl peptidase (DPP)-IV in cholestatic sepsis has not yet been reported. Common bile duct ligation (CBDL) insult was performed in adult male Sprague-Dawley rats except for sham operated animals; three doses of vildagliptin (VLD3, 10 and 30 mg/kg/d; p.o) were administered for 10 consecutive days post CBDL. VLD3/10/30 dose-dependently decreased DPP-IV and elevated GLP-1, IGF-1, PI3K, pS473-Akt (PKB), pS9-GSK-3β, pS133-CREB and cyclin-D1. VLD3/10 reduced fever, portal/aortic endotoxin and IgG, body weight loss as well as ileal NF-κB, TNF-α, MPO, TBARS, subepithelial/pericryptal and submucosal collagen deposition, vimentin immunoreactivity, N-cadherin, Zeb1 and pY654-β-catenin but increased E-cadherin, NPSH and colon/spleen indices - effects that were quite the opposite of VLD30. Accordingly, maintaining proper enterocytic proliferation/differentiation and phosphorylation inputs consequent to adequate DPP-IV inhibition is integral to AJ assembly in cholestatic sepsis; however, perturbed signals by excessive suppression of the enzyme activity induce toxic effects manifested as AJ disassembly and EMT, hence gut leakage and overt endotoxemia.

Zaky, D. A., D. M. Abouelfadl, N. N. Nassar, D. M. Abdallah, and M. Y. Al-Shorbagy, "The paradox of dipeptidyl peptidase IV inhibition in enterocytic differentiation and epithelial-mesenchymal transition in rat cholestatic sepsis.", Toxicology and applied pharmacology, vol. 394, pp. 114956, 2020. Abstract

Proper enterocytic proliferation/differentiation, besides providing adequate adherens junctions (AJ) integrity, are responsible for strengthening of the gut barrier that acts as a first line defense against endotoxemia. However, the preferential role of the underlying PI3K/Akt (PKB) axis in triggering enterocytic proliferation/differentiation signaling and AJ assembly is still obscure in sepsis. Additionally, the potential involvement of dipeptidyl peptidase (DPP)-IV in cholestatic sepsis has not yet been reported. Common bile duct ligation (CBDL) insult was performed in adult male Sprague-Dawley rats except for sham operated animals; three doses of vildagliptin (VLD3, 10 and 30 mg/kg/d; p.o) were administered for 10 consecutive days post CBDL. VLD3/10/30 dose-dependently decreased DPP-IV and elevated GLP-1, IGF-1, PI3K, pS473-Akt (PKB), pS9-GSK-3β, pS133-CREB and cyclin-D1. VLD3/10 reduced fever, portal/aortic endotoxin and IgG, body weight loss as well as ileal NF-κB, TNF-α, MPO, TBARS, subepithelial/pericryptal and submucosal collagen deposition, vimentin immunoreactivity, N-cadherin, Zeb1 and pY654-β-catenin but increased E-cadherin, NPSH and colon/spleen indices - effects that were quite the opposite of VLD30. Accordingly, maintaining proper enterocytic proliferation/differentiation and phosphorylation inputs consequent to adequate DPP-IV inhibition is integral to AJ assembly in cholestatic sepsis; however, perturbed signals by excessive suppression of the enzyme activity induce toxic effects manifested as AJ disassembly and EMT, hence gut leakage and overt endotoxemia.

Zaky, D. A., D. M. Abouelfadl, N. N. Nassar, D. M. Abdallah, and M. Y. Al-Shorbagy, "The paradox of dipeptidyl peptidase IV inhibition in enterocytic differentiation and epithelial-mesenchymal transition in rat cholestatic sepsis.", Toxicology and applied pharmacology, vol. 394, pp. 114956, 2020. Abstract

Proper enterocytic proliferation/differentiation, besides providing adequate adherens junctions (AJ) integrity, are responsible for strengthening of the gut barrier that acts as a first line defense against endotoxemia. However, the preferential role of the underlying PI3K/Akt (PKB) axis in triggering enterocytic proliferation/differentiation signaling and AJ assembly is still obscure in sepsis. Additionally, the potential involvement of dipeptidyl peptidase (DPP)-IV in cholestatic sepsis has not yet been reported. Common bile duct ligation (CBDL) insult was performed in adult male Sprague-Dawley rats except for sham operated animals; three doses of vildagliptin (VLD3, 10 and 30 mg/kg/d; p.o) were administered for 10 consecutive days post CBDL. VLD3/10/30 dose-dependently decreased DPP-IV and elevated GLP-1, IGF-1, PI3K, pS473-Akt (PKB), pS9-GSK-3β, pS133-CREB and cyclin-D1. VLD3/10 reduced fever, portal/aortic endotoxin and IgG, body weight loss as well as ileal NF-κB, TNF-α, MPO, TBARS, subepithelial/pericryptal and submucosal collagen deposition, vimentin immunoreactivity, N-cadherin, Zeb1 and pY654-β-catenin but increased E-cadherin, NPSH and colon/spleen indices - effects that were quite the opposite of VLD30. Accordingly, maintaining proper enterocytic proliferation/differentiation and phosphorylation inputs consequent to adequate DPP-IV inhibition is integral to AJ assembly in cholestatic sepsis; however, perturbed signals by excessive suppression of the enzyme activity induce toxic effects manifested as AJ disassembly and EMT, hence gut leakage and overt endotoxemia.

Zaky, D. A., D. M. Abouelfadl, N. N. Nassar, D. M. Abdallah, and M. Y. Al-Shorbagy, "The paradox of dipeptidyl peptidase IV inhibition in enterocytic differentiation and epithelial-mesenchymal transition in rat cholestatic sepsis", Toxicol Appl Pharmacol. , vol. 394, pp. 114956, 2020.
Zaky, D., D. Aboulfadl, N. Nassar, D. Abdallah, and M. Al Shorbagy, "The paradox of dipeptidyl peptidase IV inhibition in enterocytic differentiation and epithelial-mesenchymal transition in rat cholestatic sepsis", Toxicology and Applied Pharmacology, vol. 394, 2020.
Das, S., and I. A. Elhusseiny, "Paradox of Austerity: Multi-Country Evidence", Emerging Markets Finance and Trade, vol. 55, issue 8, pp. 1681-1693, 2019.
, "Paradigms of Revolutions: Political Affinities between Al Sharqawi’s Orabi: The Leader of the Peasants and the 25th of January Revolution", Creativity and Revolution Proceedings of the 11th International Symposium on Comparative Literature , English Department Cairo University, 2012, 2014. last_version_paradigms_of_revolutions.doc
, "Paradigms of Revolutions: Political Affinities between Al Sharqawi’s Orabi: The Leader of the Peasants and the 25th of January Revolution", Creativity and Revolution Proceedings of the 11th International Symposium on Comparative Literature , English Department Cairo University, 2012, 2014. last_version_paradigms_of_revolutions.doc
Iivari, J., "A paradigmatic analysis of contemporary schools of {IS} development", European Journal of Information Systems, vol. 1, pp. 249–272, 1991. Abstract
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Kattaria, T. Y., A. H. A. Mahmoud, and A. F. Wanas, "A paradigm shift: Generation of open innovation framework for building industry", Journal of Engineering and Applied Science, vol. 66, issue 2, pp. 179-198, 2019.
Mahmoud, A. H. A., T. Kattaria, and A. Wanas, "A PARADIGM SHIFT: GENERATION OF OPEN INNOVATION FRAMEWORK FOR BUILDING INDUSTRY", Journal of Engineering and Applied Science, vol. 66, issue 2, pp. 179-198, 2019.
Wahdan, A. S., G. E. Loza, H. O. Alshehri, A. F. Shedid, A. K. Salama, and W. S. Wahdan, "Paracetamol Versus Ondansetron for Prevention of Postoperative Shivering in Liposuction Surgeries Under Combined General Epidural Anaesthesia: A Randomized Controlled Trial", Turkish journal of anaesthesiology & reanimation, vol. 51, issue 3, pp. 199-206, 2033.
Abdel-Aziz, H. M., R. S. Farag, and S. A. Abdel-Gawad, "Paracetamol removal by bimetallic zero-valent Fe/Cu with benjamina leaf extract", Journal of Environmental Engineering and Science , vol. 15, issue 3, pp. 119-129, 2020.
Momenah, M. A., H. A. Ebrahim, N. M. Alzamil, M. Alfaifi, M. Y. Alshahrani, S. S. Kamar, M. A. Haidara, B. Al-Ani, and A. F. Dawood, "Paracetamol Poisoning Induces Acute Liver Injury in Rats: Inhibition of miR-155/CD45 Axis-Mediated Antioxidant Depletion and Hepatotoxicity Using Quercetin and Resveratrol", Int. J. Morphol, vol. 40, issue 5, pp. 1174-1180, 2022.
Hekal, H., A. Elkomy, M. Aboubakr, A. Soliman, A. Abdeen, and A. Abdelkader, "Paracetamol induced hepatic toxicity and amelioration by cinnamon in rats", International Journal of Pharmacology and Toxicology, vol. 4, issue 2, pp. 187 - 190, 2016. cinnamon_and_paracetamol_toxicity..pdf
Khalil, N., I. Bamil, O. Ahmed, and E. Shalaby, Paracetamol in hepatosplenic bilharziasis., , 1981. Abstract
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Kamel, N. M., D. M. El-Tanbouly, D. M. Abdallah, and H. M. Sayed, "PAR1, a therapeutic target for remote lung injury associated with hind limb ischemia/reperfusion: ERK5/KLF2-dependent lung capillary barrier preservation.", Chemico-biological interactions, vol. 354, pp. 109809, 2022. Abstract

Protease-activated receptor 1 (PAR1) is expressed in pneumocytes and endothelial cells of the alveolar barrier. Its activation by thrombin disrupts the barrier integrity dynamics and induces lung injury in in vitro and in vivo paradigms. Nonetheless, the role of PAR1, as a therapeutic target, in hind limb ischemia/reperfusion (I/R)-mediated remote lung injury has been unclear. Therefore, this study aimed to determine the potential benefit of PAR1 blockade using the selective antagonist SCH79797 in distant lung dysfunction following hind limb I/R injury with special emphasis on the extracellular signal-regulated kinase 5 (ERK5)/Krüppel-like factor 2 (KLF2) axis. Rats were subdivided into control, bilateral hind limb I/R, SCH79797, and SCH79797+BIX02189 (ERK5 inhibitor) groups. PAR1 blockade, ERK5-dependently, alleviated alveolar barrier disruption as evidenced by reductions in both pulmonary systemic leakage of surfactant protein-D and lung fluid accumulation with increase in pulmonary claudin 5, vascular endothelial cadherin, and connexin 37 levels. Such improvements are downstream targets of the ERK5/KLF2-mediated sphingosine-1-phosphate receptor 1 (S1PR1) upregulated expression and pS536-nuclear factor-κB (NF-κB) p65 inhibition. SCH79797 effectively impedes the evoked inflammatory response and oxidative burst by suppressing vascular endothelial growth factor, tumor necrosis factor-α, lipid peroxidation, and neutrophil infiltration while boosting the glutathione antioxidant defense. Accordingly, PAR1 could be a therapeutic target, where its blockade mitigated pulmonary-endothelial barrier disruption via mutual S1PR1 enhancement and NF-κB p65 inhibition following ERK5/KLF2 activation.

Kamel, N. M., D. M. El-Tanbouly, D. M. Abdallah, and H. M. Sayed, "PAR1, a therapeutic target for remote lung injury associated with hind limb ischemia/reperfusion: ERK5/KLF2-dependent lung capillary barrier preservation", Chemico-Biological Interactions, vol. 354, pp. 109809, 2022.
Kamel, N. M., D. M. El-Tanbouly, D. M. Abdallah, and H. M. Sayed, "PAR1, a therapeutic target for remote lung injury associated with hind limb ischemia/reperfusion: ERK5/KLF2-dependent lung capillary barrier preservation", Chem Biol Interact , vol. 354, pp. 109809, 2022.
A, G. K., F. M. Zahran, F. HM, and B. RS., "Papillon-Lefevre syndrome: Neutrophil function in 15 cases from 4 families in Egypt. ", Oral Surgery Oral Medicine Oral Pathology. , vol. 88, issue 3, pp. 320-325, 1999.
El Darouti, M. A., S. M. Al Raubaie, and M. A. Eiada, "Papillon-Lefévre Syndrome", International journal of dermatology, vol. 27, no. 1: Wiley Online Library, pp. 63–66, 1988. Abstract
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Tourism