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Mmalaka, "DAMAT RÜSTEM PASHA KHANS IN ISTANBUL: A STUDY OF THE ARCHITECTURE HISTORY", Othello's Island 2018: 6th conference on medieval studies, Nicosia, Cyprus, 23-27 march, 2018.
Malaka, M., and M. H. Alhaddad, "DAMAT RÜSTEM PASHA KHANS IN ISTANBUL: A STUDY OF THE ARCHITECTURE HISTORY", Othello's Island 2018: the 6th international conference on medieval studies, Cyprus, 23-27 march, 2018.
Zou, K., S. Zhu, M. R. Meselhy, C. Tohda, S. Cai, and K. Komatsu, "Dammarane-Type Saponins from Panax j aponicus and Their Neurite Outgrowth Activity in SK-N-SH Cells", Journal of natural products, vol. 65, issue 9: American Chemical Society, pp. 1288-1292, 2002. Abstract
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Nakamura, N., S. Kojima, Y. A. Lim, M. R. Meselhy, M. Hattori, M. P. Gupta, and M. Correa, "Dammarane-type triterpenes from Cordia spinescens", Phytochemistry, vol. 46, issue 6: Pergamon, pp. 1139-1141, 1997. Abstract
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El-Anwar, H. H., H. M. Serror, and S. H. Sayed, "Damping Identification Procedure for Linear Systems: Mixed Numerical-Experimental Approach", Earthquakes and Structures, an International Journal, Techno Press, vol. 4, issue 2, pp. 203-217, 2013.
El-Anwar, H. H., M. H. Serror, and H. S. Sayed, "Damping identification procedure for linear systems: mixed numerical-experimental approach", EARTHQUAKES AND STRUCTURES, vol. 4, no. 2: TECHNO-PRESS PO BOX 33, YUSEONG, DAEJEON 305-600, SOUTH KOREA, pp. 203–217, 2013. Abstract
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Hussein, T., M. S. Saad, A. L. Elshafei, and A. Bahgat, "Damping inter-area modes of oscillation using an adaptive fuzzy power system stabilizer", Electric Power Systems Research, vol. 80, no. 12: Elsevier, pp. 1428–1436, 2010. Abstract
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Oraby, M. A., M. F. El-Yamany, M. M. Safar, N. A. G. L. A. A. ASSAF, and H. A. Ghoneim, "Dapagliflozin Attenuates Early Markers of Diabetic Nephropathy in Fructose-Streptozotocin-Induced Diabetes in Rats ", Biomedicine & Pharmacotherapy, vol. 109, pp. 910–920. , 2019.
El-Yamany, M. F., M. A. Oraby, M. M. Safar, N. A. G. L. A. A. ASSAF, and H. A. Ghoneim, "Dapagliflozin attenuates early markers of diabetic nephropathy in fructosestreptozotocin- induced diabetes in rats", Biomedicine & Pharmacotherapy, vol. 109, pp. 910-920, 2019.
El-Safty, H., A. Ismail, R. Mohsen, A. E. El-Sahar, and M. Asaad, "Dapagliflozin diminishes memory and cognition impairment in Streptozotocin induced diabetes through its effect on Wnt/β-Catenin and CREB pathway", Brain Research Bulletin, vol. 181, pp. 109-120, 2022. AbstractWebsite
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El-Safty, H., A. Ismail, R. M. Abdelsalam, A. E. El-Sahar, and M. A. Saad, "Dapagliflozin diminishes memory and cognition impairment in Streptozotocin induced diabetes through its effect on Wnt/β-Catenin and CREB pathway.", Brain research bulletin, vol. 181, pp. 109-120, 2022. Abstract

Diabetic neuropathy is a chronic condition that affects a significant number of individuals with diabetes. Streptozotocin injection intraperitoneally to rodents produces pancreatic islet β-cell destruction causing hyperglycemia, which affect the brain leading to memory and cognition impairment. Dapagliflozin may be able to reverse beta-cell injury and alleviate this impairment. This effect may be via neuroprotective effect or possible involvement of the antioxidant, and anti-apoptotic properties. Forty rats were divided into four groups as follows: The normal control group, STZ-induced diabetes group, STZ-induced diabetic rats followed by treatment with oral dapagliflozin group and normal rats treated with oral dapagliflozin. Behavioral tests (Object location memory task and Morris water maze) were performed. Serum biomarkers (blood glucose and insulin) were measured and then the homeostatic model assessment for insulin resistance (HOMA-IR) was calculated. In the hippocampus the followings were determined; calmodulin, ca-calmodulin kinase Ⅳ (CaMKIV), protein kinase A (PKA) and cAMP-responsive element-binding protein to determine the transcription factor CREB and its signaling pathway also Wnt signaling pathway and related parameters (WnT, B-catenin, lymphoid enhancer binding factor LEF, glycogen synthase kinase 3β). Moreover, nuclear receptor-related protein-1, acetylcholine and its hydrolyzing enzyme acetylcholine esterase, oxidative stress parameter malondialdehyde (MDA) and apoptotic parameter caspase-3 were determined. STZ was able to cause destruction to pancreatic β-cells which was reflected on glucose levels causing diabetes. Diabetic neuropathy was clear in the rats performing the behavioral tests. Memory and cognition parameters in the hippocampus were negatively affected. Oxidative stress and apoptotic parameter were elevated while the electrical activity was declined. Dapagliflozin was able to reverse the previously mentioned parameters and behavior. Thus, to say dapagliflozin significantly showed neuroprotective action along with antioxidant, and anti-apoptotic properties.

El-Safty, H., A. Ismail, R. M. Abdelsalam, A. E. El-Sahar, and M. A. Saad, "Dapagliflozin diminishes memory and cognition impairment in Streptozotocin induced diabetes through its effect on Wnt/β-Catenin and CREB pathway.", Brain research bulletin, vol. 181, pp. 109-120, 2022. Abstract

Diabetic neuropathy is a chronic condition that affects a significant number of individuals with diabetes. Streptozotocin injection intraperitoneally to rodents produces pancreatic islet β-cell destruction causing hyperglycemia, which affect the brain leading to memory and cognition impairment. Dapagliflozin may be able to reverse beta-cell injury and alleviate this impairment. This effect may be via neuroprotective effect or possible involvement of the antioxidant, and anti-apoptotic properties. Forty rats were divided into four groups as follows: The normal control group, STZ-induced diabetes group, STZ-induced diabetic rats followed by treatment with oral dapagliflozin group and normal rats treated with oral dapagliflozin. Behavioral tests (Object location memory task and Morris water maze) were performed. Serum biomarkers (blood glucose and insulin) were measured and then the homeostatic model assessment for insulin resistance (HOMA-IR) was calculated. In the hippocampus the followings were determined; calmodulin, ca-calmodulin kinase Ⅳ (CaMKIV), protein kinase A (PKA) and cAMP-responsive element-binding protein to determine the transcription factor CREB and its signaling pathway also Wnt signaling pathway and related parameters (WnT, B-catenin, lymphoid enhancer binding factor LEF, glycogen synthase kinase 3β). Moreover, nuclear receptor-related protein-1, acetylcholine and its hydrolyzing enzyme acetylcholine esterase, oxidative stress parameter malondialdehyde (MDA) and apoptotic parameter caspase-3 were determined. STZ was able to cause destruction to pancreatic β-cells which was reflected on glucose levels causing diabetes. Diabetic neuropathy was clear in the rats performing the behavioral tests. Memory and cognition parameters in the hippocampus were negatively affected. Oxidative stress and apoptotic parameter were elevated while the electrical activity was declined. Dapagliflozin was able to reverse the previously mentioned parameters and behavior. Thus, to say dapagliflozin significantly showed neuroprotective action along with antioxidant, and anti-apoptotic properties.

El-Sahar, A. E., A. A. Rastanawi, M. F. El-Yamany, and M. Asaad, "Dapagliflozin improves behavioral dysfunction of Huntington's disease in rats via inhibiting apoptosis-related glycolysis", Life Sciences, vol. 257, 2020. AbstractWebsite
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El-Sahar, A. E., A. A. Rastanawi, M. F. El-Yamany, and M. A. Saad, "Dapagliflozin improves behavioral dysfunction of Huntington's disease in rats via inhibiting apoptosis-related glycolysis.", Life sciences, vol. 257, pp. 118076, 2020. Abstract

AIMS: Huntington's disease is a rare neurodegenerative disorder which is associated with defected glucose metabolism with consequent behavioral disturbance including memory and locomotion. 3-nitropropionic acid (3-NP) can cause, in high single dose, an acute striatal injury/Huntington's disease. Dapagliflozin, which is one of the longest duration of action of SGLTIs family, may be able to diminish that injury and its resultant behavioral disturbances.

MATERIAL AND METHODS: Forty rats were divided into four groups (n = 10 in each group): normal control group (CTRL), dapagliflozin (CTRL + DAPA) group, 3-nitropropionic acid (3-NP) group, and dapagliflozin plus 3-nitropropionic acid (DAPA + 3-NP) group. Behavioral tests (beam walking test, hanging wire test, limb withdrawal test, Y-maze spontaneous alteration, elevated plus maze) were performed with evaluating neurological scoring. In striatum, neurotransmitters (glutamate, aspartate, GABA, ACh and AChE activity) were measured. In addition, apoptosis and glycolysis markers (NF-κB, Cyt-c, lactate, HK-II activity, P53, calpain, PEA15 and TIGAR) were determined. Inflammation (IL-1β, IL-6, IL-8 and TNF-α) and autophagy (beclin-1, LC3 and DRAM) indicators were measured. Additionally, histopathological screening was conducted.

KEY FINDINGS: 3-Nitropropionic acid had the ability to perturb the neurotransmission which was reflected in impaired behavioral outcome. All of glycolysis, apoptosis and inflammation markers were elevated after 3-NP acute intoxication but autophagy parameters, except DRAM, were reduced. However, DAPA markedly reversed the abovementioned parameters.

SIGNIFICANCE: Dapagliflozin demonstrated anti-glycolytic, anti-apoptotic, anti-inflammatory and autophagic effects on 3-NP-damaged striatal cells and promoted the behavioral outcome.

Sayed, R. H., M. Asaad, and A. E. El-Sahar, "Dapoxetine attenuates testosterone-induced prostatic hyperplasia in rats by the regulation of inflammatory and apoptotic proteins", Toxicology and Applied Pharmacology, vol. 311, pp. 52-60, 2016. AbstractWebsite
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Sayed, R. H., M. A. Saad, and A. E. El-Sahar, "Dapoxetine attenuates testosterone-induced prostatic hyperplasia in rats by the regulation of inflammatory and apoptotic proteins.", Toxicology and applied pharmacology, vol. 311, pp. 52-60, 2016 Nov 15. Abstract

Serotonin level plays a role in suppressing the pathological findings of benign prostatic hyperplasia (BPH). Thus a new selective serotonin reuptake inhibitor, dapoxetine was used to test its ability to ameliorate the pathological changes in the rat prostate. A dose response curve was constructed between the dose of dapoxetine and prostate weight as well as relative prostate weight, then a 5mg/kg dose was used as a representative dose for dapoxetine administration. Rats were divided into four groups; the control group that received the vehicle; the BPH-induced group received daily s.c injection of 3mg/kg testosterone propionate dissolved in olive oil for four weeks; BPH-induced group treated with finasteride 5mg/kg/day p.o and BPH-induced group treated with dapoxetine 5mg/kg/day p.o. Injection of testosterone increased prostate weight and relative prostate weight which were both returned back to the normal value after treatment with dapoxetine as well as finasteride. Testosterone also upregulated androgen receptor (AR) and proliferating cell nuclear antigen gene expression. Furthermore, testosterone injection elevated cyclooxygenase-II (COX II), inducible nitric oxide synthase (iNOS), B-cell lymphoma-2 (Bcl2) expression and tumor necrosis factor alpha content and reduced caspase-3 activity, Bcl-2-associated X protein (Bax) expression and Bax/Bcl2 ratio. Dapoxetine and finasteride administration reverted most of the changes made by testosterone injection. In conclusion, the current study provides an evidence for the protective effects of dapoxetine against testosterone-induced BPH in rats. This can be attributed, at least in part, to decreasing AR expression, and the anti-proliferative, anti-inflammatory and pro-apoptotic activities of dapoxetine in BPH.

Sayed, R. H., M. A. Saad, and A. E. El-Sahar, "Dapoxetine attenuates testosterone-induced prostatic hyperplasia in rats by the regulation of inflammatory and apoptotic proteins.", Toxicology and applied pharmacology, vol. 311, pp. 52-60, 2016 Nov 15. Abstract

Serotonin level plays a role in suppressing the pathological findings of benign prostatic hyperplasia (BPH). Thus a new selective serotonin reuptake inhibitor, dapoxetine was used to test its ability to ameliorate the pathological changes in the rat prostate. A dose response curve was constructed between the dose of dapoxetine and prostate weight as well as relative prostate weight, then a 5mg/kg dose was used as a representative dose for dapoxetine administration. Rats were divided into four groups; the control group that received the vehicle; the BPH-induced group received daily s.c injection of 3mg/kg testosterone propionate dissolved in olive oil for four weeks; BPH-induced group treated with finasteride 5mg/kg/day p.o and BPH-induced group treated with dapoxetine 5mg/kg/day p.o. Injection of testosterone increased prostate weight and relative prostate weight which were both returned back to the normal value after treatment with dapoxetine as well as finasteride. Testosterone also upregulated androgen receptor (AR) and proliferating cell nuclear antigen gene expression. Furthermore, testosterone injection elevated cyclooxygenase-II (COX II), inducible nitric oxide synthase (iNOS), B-cell lymphoma-2 (Bcl2) expression and tumor necrosis factor alpha content and reduced caspase-3 activity, Bcl-2-associated X protein (Bax) expression and Bax/Bcl2 ratio. Dapoxetine and finasteride administration reverted most of the changes made by testosterone injection. In conclusion, the current study provides an evidence for the protective effects of dapoxetine against testosterone-induced BPH in rats. This can be attributed, at least in part, to decreasing AR expression, and the anti-proliferative, anti-inflammatory and pro-apoptotic activities of dapoxetine in BPH.

Sayed, R. H., M. A. Saad, and A. E. El-Sahar, "Dapoxetine attenuates testosterone-induced prostatic hyperplasia in rats by the regulation of inflammatory and apoptotic proteins.", Toxicology and applied pharmacology, vol. 311, pp. 52-60, 2016 Nov 15. Abstract

Serotonin level plays a role in suppressing the pathological findings of benign prostatic hyperplasia (BPH). Thus a new selective serotonin reuptake inhibitor, dapoxetine was used to test its ability to ameliorate the pathological changes in the rat prostate. A dose response curve was constructed between the dose of dapoxetine and prostate weight as well as relative prostate weight, then a 5mg/kg dose was used as a representative dose for dapoxetine administration. Rats were divided into four groups; the control group that received the vehicle; the BPH-induced group received daily s.c injection of 3mg/kg testosterone propionate dissolved in olive oil for four weeks; BPH-induced group treated with finasteride 5mg/kg/day p.o and BPH-induced group treated with dapoxetine 5mg/kg/day p.o. Injection of testosterone increased prostate weight and relative prostate weight which were both returned back to the normal value after treatment with dapoxetine as well as finasteride. Testosterone also upregulated androgen receptor (AR) and proliferating cell nuclear antigen gene expression. Furthermore, testosterone injection elevated cyclooxygenase-II (COX II), inducible nitric oxide synthase (iNOS), B-cell lymphoma-2 (Bcl2) expression and tumor necrosis factor alpha content and reduced caspase-3 activity, Bcl-2-associated X protein (Bax) expression and Bax/Bcl2 ratio. Dapoxetine and finasteride administration reverted most of the changes made by testosterone injection. In conclusion, the current study provides an evidence for the protective effects of dapoxetine against testosterone-induced BPH in rats. This can be attributed, at least in part, to decreasing AR expression, and the anti-proliferative, anti-inflammatory and pro-apoptotic activities of dapoxetine in BPH.

MM, G., A. - S. MS, and N. YM, "Dapson in heterocyclic chemistry part VI: synthesis and molecular docking of some novel sulfonebiscompounds of expected anticancer activity", Arzneimittelforschung, vol. 62, issue 11, pp. 497-507, 2012.
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