Publications

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2020
Haidara, M. A., B. Al-Ani, R. A. Eid, M. E. D. Mohammed, F. Al-Hashem, and M. Dallak, "Acetaminophen Induces Alterations to the Renal Tubular Ultrastructure in a Rat Model of Acute Nephrotoxicity Protected by Resveratrol and Quercetin", Int. J. Morphol, vol. 38, issue 3, pp. 585-591, 2020. pdf_acteom..pdf
Haidara, M. A., B. Al-Ani, R. A. Eid, M. E. D. Mohammed, F. AL-HASHEM, and M. DALLAK, "Acetaminophen Induces Alterations to the Renal Tubular Ultrastructure in a Rat Model of Acute Nephrotoxicity Protected by Resveratrol and Quercetin", Int. J. Morphol, vol. 38, issue 3, pp. 585-591, 2020.
Eid, R. A., M. S. A. Zaki, M. A. Alghamd, A. Wares, M. A. Eldeen, E. E. S. Massoud, and M. A. Haidara, "Ameliorative Effect of Vitamin E on Biochemical and Ultrastructural Changes in Artemether-induced Renal Toxicity in Rats", Int. J. Morphol, vol. 38, issue 2, pp. 461-471, 2020. sc_cu_pdf_5.pdf
Zaki, M. S. A., M. A. Haidara, M. A. Alghamd, A. A. Shati, A. Wares, and R. A. Eid, "Protective Effect of Dietary Vitamin E (a Tocopherol) on Artemisinin Induced Oxidative Liver Tissue Damage in Rats", Int. J. Morphol, vol. 38, issue 2, pp. 278-288, 2020. sc_cu_pdf_4.pdf
Eid, R. A., M. S. A. Zaki, M. A. Alghamd, A. M. Sideeg, A. Z. M. Kamal, M. Andarawi, and M. A. Haidara, "Vitamin C Administration Attenuated Artemether- Induced Hepatic Injury in Rats", Int. J. Morphol, vol. 38, issue 1, pp. 48-55, 2020. sc_3.pdf
2019
Karib, A. E. O., M. Dallak, R. A. Eid, and H. MA, "Pre-Diabetes Induces Ultrastructural Alterations in the Large Blood Vessel Aorta in Rats. ", Int. J. Morphol, vol. 37, issue 2, pp. 467-653, 2019. haidara_ijm-pdf.pdf
Dallak M, B. - J. I, S. H, and H. MA, "Swim exercise inhibits hemostatic abnormalities in a rat model of obesity and insulin resistance. ", Arch Physiol Biochem., vol. 125 , issue 1, pp. 79-84 , 2019. haidara-_archive_pdf.pdf
Dallak M, B. - J. I, S. H, and H. MA, "Swim exercise inhibits hemostatic abnormalities in a rat model of obesity and insulin resistance. ", Arch Physiol Biochem., vol. 125 , issue 1, pp. 79-84 , 2019. haidara-_archive_pdf.pdf
2018
Bin-Jaliah, I., H. F. SAKR, M. D. Morsy, M. Dallak, and M. A. Haidara, "Modulatory Effect of Concomitant Administration of Insulin and Vanadium on Inflammatory Biomarkers in Type 2 Diabetic Rats: Role of Adiponectin.", Chinese Journal of Physiology, vol. 61 , issue (1), pp. 42-49, 2018. haidara_-_cjp-_pdf.pdf
Dallak, M. A., A. A. Ismaeel Bin-Jaliah, Mohamed A. Haidara, and B. Al-Ani, "Swim exercise training ameliorates hepatocyte ultrastructural alterations in rats fed on a high fat and sugar diet", Ultrastructural Pathology, vol. 42, issue 2, pp. 155-161, 2018. haidara_ultrastruc_path___pdf.pdf
2017
Humayed, S. A., R. A. Eid, M. A. Haidara, and B. Al-Ani, "Differential Therapeutic Effects of Crataegus aronia and Simvastatin on the Hepatocyte Ultrastructure in Hepatic Steatosis", International Journal of morphology , vol. 35, issue 2, pp. 578-583, 2017. liver_statiosis_-aronia-__int_j_morphology-.pdf
Al-Hashema, F., A. E. O. Karib, M. A. Haidara, and B. Al-Ania, "Exercise protects against insulin-dependent diabetes-induced osteoarthritis in rats: A scanning electron microscopy study", ULTRASTRUCTURAL PATHOLOGY, vol. 431, issue 3, pp. 252-257, 2017. ultrastructural_pathology2c_20172c_413_252-257.pdf
Al-Hashema, F., A. E. O. Karib, M. A. Haidara, and B. Al-Ania, "Exercise protects against insulin-dependent diabetes-induced osteoarthritis in rats: A scanning electron microscopy study", ULTRASTRUCTURAL PATHOLOGY, vol. 431, issue 3, pp. 252-257, 2017. ultrastructural_pathology2c_20172c_413_252-257.pdf
2016
2015
Haidara, M. A., A. S. Assiri, M. A. Youssef, M. M. Mahmoud, E. M. Ahmed, A. Al-Hakami, and H. C. Chandramoorthy, "Differentiated mesenchymal stem cells ameliorate cardiovascular complications in diabetic rats", Cell Tissue Res, vol. 359, pp. 565–575, 2015. 2015_-stem_cell_-_haidara-_cell_tissue_research_1.pdf
Haidara, M. A., A. S. Assiri, H. Z. Yassin, H. I. Ammar, M. M. Obradovic, and E. R. Isenovic, "Heart Failure Models: Traditional and Novel Therapy", Current Vascular Pharmacology, vol. 13, issue 5, pp. 658-69., 2015. haidara-_cvp_2015_1.pdf
2014
ELEAWA, S. M., M. A. ALKHATEEB, F. H. ALHASHEM, I. Bin-Jaliah, H. F. SAKR, H. M. ELREFAEY, A. O. ELKARIB, M. A. HAIDARA, A. S. SHATOOR, and M. A. KHALIL, "Resveratrol Reverses Cadmium Chloride-induced Testicular Damage and Subfertility by Downregulating p53 and Bax and Upregulating Gonadotropins and Bcl-2 gene Expression", Journal of Reproduction and Development, vol. 60, issue 2, pp. 115-127, 2014. reg_bup_jorstmr_ltqdm_lmkf_lnshr_lmmy.pdf
2013
M1, O., B. P, R. M, K. N, H. M, S. AJ, J. A, and I. ER, "Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular diseases", J Endocrinol, vol. 18, issue 3, pp. 13-23, 2013. Abstractr13.full_.pdf

Obesity is associated with aberrant sodium/potassium-ATPase (Na(+)/K(+)-ATPase) activity, apparently linked to hyperglycemic hyperinsulinemia, which may repress or inactivate the enzyme. The reduction of Na(+)/K(+)-ATPase activity in cardiac tissue induces myocyte death and cardiac dysfunction, leading to the development of myocardial dilation in animal models; this has also been documented in patients with heart failure (HF). During several pathological situations (cardiac insufficiency and HF) and in experimental models (obesity), the heart becomes more sensitive to the effect of cardiac glycosides, due to a decrease in Na(+)/K(+)-ATPase levels. The primary female sex steroid estradiol has long been recognized to be important in a wide variety of physiological processes. Numerous studies, including ours, have shown that estradiol is one of the major factors controlling the activity and expression of Na(+)/K(+)-ATPase in the cardiovascular (CV) system. However, the effects of estradiol on Na(+)/K(+)-ATPase in both normal and pathological conditions, such as obesity, remain unclear. Increasing our understanding of the molecular mechanisms by which estradiol mediates its effects on Na(+)/K(+)-ATPase function may help to develop new strategies for the treatment of CV diseases. Herein, we discuss the latest data from animal and clinical studies that have examined how pathophysiological conditions such as obesity and the action of estradiol regulate Na(+)/K(+)-ATPase activity.

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