Basic Informations

C.V

Curriculum Vitae

Name:                             Mohammed Omar Mahmoud Ahmed Mostafa                   

Position:                         Lecturer of Biochemistry.                                                 

Military service:             Completed (Oct. 2003 – Jan. 2004).                                 

Marital status:               Married with 2 children                                                    

Nationality:                    Egyptian.                                                                          

Date of Birth:                 June 18, 1980.

Address:                         1) 5 Ahmed Abdel Hamid Street, Beni-Suef, Egypt.

2) Faculty of Pharmacy, Beni-Suef University, El Shahid Ahmed Hegazi Street, Beni-Suef, 62514, Egypt

Mobile:                           +2 010 9523434.

E-mails:                          1 - mohamed.omar@pharm.bsu.edu.eg  

                                       2- mohamed_omar_bio@yahoo.com

Degrees:                           

1)      B.Sc. of Pharmaceutical sciences (Excellent with honor degree), Cairo University, Beni-Sueif Branch, 2002.

2)      M.Sc. Biochemistry, Beni-Suef University, 2009.

3)      Ph.D. Biochemistry, Beni-Suef University, 2014.

Experiences:

1-    Demonstrator of Biochemistry, Faculty of Pharmacy, Beni-Suef University, 2004-2009.

2-    Assistant lecturer of Biochemistry, Faculty of Pharmacy, Beni-Suef University, 2009- 2014.

3-    Lecturer of Biochemistry, Faculty of Pharmacy, Beni-Suef University, 2014 till now.

Noticing that:

1- The research unit at Beni-Suef branch of Cairo University was completed at July 2002.

2- Beni-Suef University, Egypt (was separated from Cairo University according to the Republic role No [192/2005] starting 1 August 2005).

3- All courses and exams (written, oral, and practical) during undergraduate and graduate studies were in English.

Fields of research and routine work:

Research in diabetes mellitus, hepatic diseases, oxidative stress and antioxidants.

Brief description of duties:                                                                                                            

  • Teaching of Biochemistry-1 for undergraduate students of Program of pharmaceutical Science and Program of Clinical Pharmacy
  • Teaching of Biochemistry-2 for undergraduate students of Program of pharmaceutical Science and Program of Clinical Pharmacy
  • Teaching of Clinical Chemistry for undergraduate students of Program of pharmaceutical Science and Program of Clinical Pharmacy.                                                                                                                           
  • Teaching of postgraduate students special courses of Advanced Biochemistry-1,  Advanced Biochemistry-2,  Laboratory techniques, Bioorganic chemistry and Role of nutrition in disease prevention.
  • Supervision on the practical sections of undergraduates.
  • Participating in preparation of theoretical and practical exams of undergraduates.  
  • Supervision on the summer training of the undergraduates                                                                                         
  • Contributing to ongoing research program in of the Department as well as in collaboration with other University divisions and supervising the master degrees of postgraduate’s candidates.
  • Supervision on Thesis of Postgraduates.

Activities:

1)       Chef Information Officer (CIO), 12/2010 till 12/2013.

2)       Member of the Egyptian Pharmacists Syndicate.

3)       Attendance the second scientific symposium of Faculty of Pharmacy, Beni-Suef University on "Recent Advances in Pharmaceutical Research", Jan. 12th, 2011.

4)       Attendance a training workshop of molecular biology practice at faculty of pharmacy, Cairo University, 14-19 September 2011.

5)       Attendance the first international conference of Faculty Pharmacy, Beni-Suef University on "Helth between nutrition and treatment", Aug. 30th, 2015.

6)        Attendance workshop of "structural biology: the importance of understanding biology on the atomic level" in Faculty Pharmacy, Beni-Suef University, March 16th 2017.

7)       Attendance workshop of "recombinant DNA technologies for protein expression" in Faculty Pharmacy, Beni-Suef University, March 30th 2017.

8)       Attendance workshop of "protein production and crystalization" in Faculty Pharmacy, Beni-Suef University, April 16th 2017.

9)       Attendance workshop of "principle of synchrotron" in Faculty Pharmacy, Beni-Suef University, May 2th 2017.

10)  Attendance training course in Beni-Suef University "A single software that will fulfil almost all your Bioinformatics needs" May 13th, 2017.  

Thesis:

Mohamed Omar Mahmoud, (2009). Effect of Glycemic Control on Cardiovascular Dysfunction and Oxidative Stress in Type 2 Diabetes. Thesis for M.Sc. degree. Faculty of Pharmacy, Beni-Suef University.  

Mohamed Omar Mahmoud, (2014). Effect of glycemic control on soluble RAGE and oxidative stress in type 2 diabetic patients. Thesis for Ph.D. degree. Faculty of Pharmacy, Beni-Suef University.

Computer skills:

ICDL equivalent certificate, Supreme Council of Universities, Egypt, January 20, 2007.

Publication:

1- Motawi TMK, Houssen ME, Mahmoud MO, and Abou-Seif MA. Effect of Glycemic Control on Endothelial Dysfunction and Oxidative Stress in Normotensive and Hypertensive Type 2 Diabetics. The Egyptian Journal of Biochemistry and Molocular Biology. 2009:159-175.

2- Motawi TMK, Abou-Seif MA, Bader AMA and Mahmoud MO. Effect of glycemic control on soluble RAGE and oxidative stress in type 2 diabetic patients. BMC Endocrine Disorders. 2013; 13: 32.

3- Hashem RM, Hassanin KMA, LA Rashed, Mahmoud MO and Hassan MG. Effect of silibinin and vitamin E on the ASK1-p38 MAPK pathway in D-galactosamine/lipopolysaccharide induced hepatotoxicity. Exp Biol Med. 2016;241:1250-1257.

4- Mahmoud MO, Aboud HM, AH Hassan, Ali AA, Johnston TP. Transdermal delivery of atorvastatin calcium from novel nanovesicular systems using polyethylene glycol fatty acid esters: Ameliorated effect without liver toxicity in poloxamer 407-induced hyperlipidemic rats. Journal of Controlled Release 2017;254:10-22.

5- Hassanin KMA, Mahmoud MO, Hassan HM, Abdel-Razik AH, Aziz LN, Rateb ME. Balanites aegyptiaca ameliorates insulin secretion and decreases pancreatic apoptosis in diabetic rats: Role of SAPK/JNK pathway. Biomedicine & Pharmacotherapy. 2018;102:1084–1091.

6- Mohammed MA, Mahmoud MO, Awaad AS, Gamal GM, Abdelfatah D. Alpha lipoic acid protects against dexamethasone-induced metabolic abnormalities via APPL1 and PGC-1 α up regulation. Steroids. 2019;144:1-7.

7- Kandeil MA, Mahmoud MO, Abdel-Razik AH, Gomaa SB. Thymoquinone and geraniol alleviate cisplatin-induced neurotoxicity in rats through downregulating the p38 MAPK/STAT-1 pathway and oxidative stress. Life Sci. 2019;228:145-151.

8- Aboud HM, Mahmoud MO, Mohammed MA, Awad MS, Sabry D. Preparation and appraisal of self-assembled valsartan-loaded amalgamated Pluronic F127/Tween 80 polymeric micelles: Boosted cardioprotection via regulation of Mhrt/Nrf2 and Trx1 pathways in cisplatin-induced cardiotoxicity. J Drug Target. 2019;19:1-18.

9- Kandeil MA, Hashem RM, Mahmoud MO, Hetta MH, Tohamy MA. Zingiber officinale extract and omega-3 fatty acids ameliorate endoplasmic reticulum stress in a nonalcoholic fatty liver rat model. J Food Biochem. 2019;00:e13076.

 

 

Projects:

1- Principal Investigator in the collective project funded by the Beni-Suef University, entitled "Association of some genetic polymorphisms with type 2 diabetes mellitus in Egyptians", 2016. (50,000 EGP., Beni-Suef University).

2- Researcher in the project funded by the Beni-Suef University, entitled "Studying the protective effect of nanoparticles loaded with natural products combination with different mode of actions for treatment of neurodegenerative diseases", 2018. (50,000 EGP., Beni-Suef University).

 

Reviewer in some scientific journals

  • Beni-Suef University Journal of Applied Sciences
  • Pharmaceutical Development and Technology 
  • Science of the Total Environment
  • Heliyon

 

C.V PDF

Master Title

Effect of Glycemic Control on Cardiovascular Dysfunction and Oxidative Stress in Type 2 Diabetes

Master Abstract

The present study was conducted firstly, to evaluate whether an intensive glycemic control may improve both endothelial dysfunction (i.e. ADMA levels) and oxidative stress in type 2 diabetic patients with or without hypertension. Secondary, to assess the role of blood pressure regulation using ACE inhibitors on modulating endothelial dysfunction and oxidative stress in hypertensive diabetic patients. The current study was conducted in the Out-patient Clinic of Beni- Sueif University Hospital and comprising 90 subjects; 72 patients with type 2 diabetes along with 18 healthy control volunteers. Inclusion criteria for patients enrolled in the study included the following: age between 40-70 years; receiving stable antidiabetic therapy (sulfonylurea, metformin and/or insulin) for at least 6-8 months and no history of ketoacidosis. In hypertensive diabetic patients submitted to the study, the antihypertensive treatment was ACE inhibitors for at least 6-8 months. Exclusion criteria included the following: clinically significant hepatic, neurological, endocrinologic or other major systemic diseases, such as malignancy; elevated plasma transaminases activities over twice the upper normal limit; elevated plasma creatinine concentration (> 1.7 mg/dl); acute major cardiovascular events in the previous 6 months; acute illnesses; current evidence of acute or chronic inflammatory diseases and hormone replacement therapy for women subjected to the study. Exclusion criteria also included anemia, hyperbilirubinemia, treatment with glucocorticoids, antineoplastic agents, psychoactive agents, bronchodilators, statins or vitamin supplements. The patients enrolled in the present study were classified into the following groups according to presence or absence of hypertension and glycemic control where the patients were subdivided into good glycemic control (HbA1C = 7.0 %) and poor glycemic control (HbA1C > 7.0 %) along with normal subjects: / 2317953 / ? ? ??? ??/ ????? ?? ?? ????? – ? ?? ?? ?? ? ? : 2317958 ?: 2319397 2317950 Web site: www.pharm.bsu.edu.eg Mail: pharm@bsu.edu.eg Group (1) (control group): included eighteen healthy individuals. Group (2): included eighteen normotensive good controlled diabetic patients. Group (3): included eighteen normotensive poorly controlled diabetic patients. Group (4): included eighteen hypertensive good controlled diabetics treated with ACE inhibitors. Group (5): included eighteen hypertensive poorly controlled diabetics treated with ACE inhibitors. Five milliliters of venous blood samples were withdrawn after 12- 14 hours overnight fast from each subject enrolled in the study. Each blood sample was collected into tubes containing EDTA and divided into 2 aliquots. The first aliquot was of 1.5 ml whole blood used for estimation of GSH, HbA1C and blood hemoglobin. The second aliquot was of 3.5 ml blood centrifuged at 2000 x g for 10 minutes to obtain plasma for estimation of plasma glucose, plasma total bilirubin, plasma creatinine, lipid profile and plasma MDA levels, AST and ALT activities. The remaining plasma was stored at –20ºC for subsequent estimation of plasma ADMA levels. The present study showed a significant increase in FPG levels and HbA1C levels in normotensive and hypertensive diabetics compared with normal control. In addition, there was a significant increase in FPG levels and HbA1C levels in normotensive and hypertensive poorly controlled diabetics compared with normotensive and hypertensive good controlled diabetics, respectively. The increased HbA1C levels may be attributed to the intracellular hyperglycemia which increases non-enzymatic attachment of glucose molecules to primary amino groups of hemoglobin protein, forming a stable Amadori products such as the HbA1C adduct in normotensive and hypertensive poorly controlled diabetics. The decreased FPG and HbA1C levels in normotensive and hypertensive good controlled diabetics is mainly due to intensive glycemic control via hypoglycemic drugs. ACE inhibitors may partly influence glycemic control in hypertensive diabetics through vasodilatation which may promote an access of glucose and insulin into skeletal muscle tissue, the main target organ for insulin action. Fasting plasma glucose levels were correlated with HbA1C levels in all diabetic groups in the current study. / 2317953 / ? ? ??? ??/ ????? ?? ?? ????? – ? ?? ?? ?? ? ? : 2317958 ?: 2319397 2317950 Web site: www.pharm.bsu.edu.eg Mail: pharm@bsu.edu.eg The present study showed a significant decrease in plasma ADMA levels in normotensive and hypertensive diabetics compared with normal control. The decreased ADMA levels in normotensive and hypertensive poorly controlled diabetic patients is attributed to increased renal excretion that results from increased glomerular filtration rate while decreased ADMA levels in normotensive and hypertensive good controlled diabetics was attributed to increased degradation by DDAH enzyme. ACE inhibitors may also decrease plasma ADMA levels in hypertensive diabetics. Plasma ADMA levels were correlated with both plasma MDA and blood GSH levels in all diabetic groups, supporting the relationship between ADMA and oxidative stress. The present work showed a significant increase in plasma MDA levels in normotensive and hypertensive diabetics compared with normal control. In addition, there was a significant increase in MDA levels in normotensive and hypertensive poorly controlled diabetics compared with normotensive and hypertensive good controlled diabetics, respectively. In diabetes, there is an increased production of free radicals, which in turn promotes lipid peroxidation with the formation of MDA the end product of lipid peroxidation. The decreased MDA levels in normotensive and hypertensive good controlled diabetics may be a consequence of intensive glycemic control reflected by low HbA1C levels and also due to antioxidant properties of hypoglycemic drugs used in treatment of diabetes. The antioxidant effect of ACE inhibitors may also contribute to decreased MDA levels in hypertensive diabetics. Significant correlation was found between plasma MDA and GSH levels in all diabetic groups in the present investigation. The current work found a significant decrease in blood GSH levels in normotensive and hypertensive diabetics compared with normal control. In addition, there was a significant decrease in GSH levels in normotensive and hypertensive poorly controlled diabetics compared with normotensive and hypertensive good controlled diabetics, respectively. The decreased GSH level in diabetics may be caused by increased sorbitol synthesis which leads to NADPH depletion, and limits reduction of GSSG to GSH catalyzed by glutathione reductase. Also, decreased activity of enzymes involved in pentose phosphate pathway which generates NADPH in diabetics, so reduction of GSSG is limited and finally, GSSG can pass through erythrocyte membrane due to oxidative stress-induced membrane damage. In addition to effect of intensive glycemic / 2317953 / ? ? ??? ??/ ????? ?? ?? ????? – ? ?? ?? ?? ? ? : 2317958 ?: 2319397 2317950 Web site: www.pharm.bsu.edu.eg Mail: pharm@bsu.edu.eg control, the effect of hypoglycemic drugs on improving antioxidant status may contribute to increased GSH levels in normotensive and hypertensive good controlled diabetics compared with those normotensive and hypertensive poorly controlled diabetics. In hypertensive diabetics, the treatment with ACE inhibitors which possess antioxidant properties may also contribute to enhancement of GHS levels. A negative correlation between blood GSH and HbA1C levels in all diabetic groups was found. No significant difference was observed in all measured parameters in the present study when comparing normotensive with hypertensive diabetics which may be attributed to the use of ACE inhibitors in treatment of hypertensive diabetics, so their parameter levels become similar to those in normotensive diabetics. From the present study we can conclude firstly, that there is a relevant relationship between glycemic control, oxidative stress and endothelial dysfunction. Secondary, that diabetes-associated conditions such as hypertension may result in an increased cellular production of reactive oxygen species which impairs endothelial function. Finally and more importantly, besides the role of antidiabetic drugs and ACE inhibitors in modulating glycemic control and regulating hypertension respectively, they have great antioxidant activities which affect endothelial function and oxidative status in diabetic patients. Further studies are needed to investigate the effect of different hypoglycemic drugs on DDAH activity as a mechanism that lowers ADMA levels in diabetic patients and to investigate the antioxidant properties of these drugs which may be of benefit in delaying diabetic complications. Also, to investigate the role of blood pressure-lowering effect of antihypertensive drugs in modulation of oxidative stress and endothelial dysfunction.

Master Abstract PDF

PHD Title

Effect of Glycemic Control on Soluble RAGE and Oxidative Stress in Type 2 Diabetic Patients

PHD Abstract

The present study was designed to evaluate the effect of glycemic control on soluble receptor of advanced glycation end product (sRAGE) and some oxidative stress markers in type 2 diabetic patients. This study was conducted in the Out-patient Clinic of Beni-Suef University Hospital between September 2011 and June 2012 and comprising 90 subjects who were subdivided into 20 healthy control volunteers and 70 patients with type 2 diabetes mellitus (T2DM). All patients enrolled in the study fulfilled the following criteria: age between 35-70 years; receiving stable antidiabetic therapy (sulfonylurea, metformin, thiazoldinedione and/or insulin) for at least 6-8 months and no history of ketoacidosis. In hypertensive diabetic patients submitted to the study, the antihypertensive treatments were angiotensin converting enzyme inhibitors, angiotensin receptor blockers, Ca2+ channel blockers, ß-blockers and/or diuretics for at least 6-8 months. Exclusion criteria included the following: clinically significant hepatic, neurological, endocrinologic or other major systemic diseases, such as malignancy; elevated plasma transaminase activities over twice the upper limit of normal; elevated plasma creatinine concentrations (>150 µmol/L or 1.7 mg/dl); acute major cardiovascular events in the previous 6 months; acute illnesses; current evidence of acute or chronic inflammatory diseases and hormone replacement therapy for women subjected to the study. Exclusion criteria also included treatment with glucocorticoids, antineoplastic agents, psychoactive agents, bronchodilators, statins or vitamin supplements. The patients enrolled in the present study were classified according to glycemic control [good glycemic control (glycated hemoglobin (HbA1c) = 7.0 %) and poor glycemic control (HbA1c > 7.0 %)] with or without hypertension (SBP > 140 mmHg or DBP > 90 mmHg) along with normal subjects as follows: I- Control healthy subjects [Group (1)]: It included twenty healthy individuals, age– and body mass index (BMI)–matched with diabetic patients. II- Good controlled diabetics [Group (2)]: It was composed of twenty eight good controlled diabetics (GCD). III- Poorly controlled diabetics [Group (3)]: It was composed of forty two poorly controlled diabetics (PCD). Ten milliliters of venous blood samples were withdrawn after 12-14 hours overnight fast from each subject enrolled in the study. Each blood sample was collected into tubes containing EDTA and divided into 2 aliquots. The first aliquot was of 4 ml whole blood used for estimation of glutathione (GSH), HbA1c and superoxide dismutase (SOD) activity. The second aliquot was of 6 ml blood centrifuged at 2000 x g for 10 minutes to obtain plasma for estimation of plasma glucose levels, alanine transaminase (ALT) and aspartate transaminase (AST) activities, plasma creatinine and lipid profile. The remaining plasma was stored at –20ºC for subsequent estimation of C-peptide, sRAGE, vascular cell adhesion molecule-1(VCAM-1), oxidized low density lipoprotein (ox-LDL) and total nitric oxide (NOx) levels. The present study showed a significant increase in fasting plasma glucose (FPG) levels in both diabetic groups compared with normal controls and increased HbA1c levels in PCD compared with GCD. The increase in HbA1c is attributable to the intracellular hyperglycemia which increases non-enzymatic attachment of glucose molecules to primary amino groups of hemoglobin protein, forming stable Amadori products such as the HbA1c adduct. Additionally, a significant positive correlation was found between HbA1c and FPG levels in all diabetic patients in the current study. The lower FPG and HbA1c levels in GCD compared with PCD may be attributed to intensive glycemic control with different hypoglycemic drugs such as sulfonylureas and metformin. The current work showed a significant decrease in sRAGE levels in PCD compared with normal control. Moreover, no significant difference in the mean plasma sRAGE levels was observed when comparing GCD with either PCD or with normal control. The sRAGE level in PCD may be reduced due to excessive binding to circulating AGEs ligands. Increased ligand burden may consume all existing sRAGE and/or endogenous mechanisms that release sRAGE may be impaired. The plasma VCAM-1 levels showed a significant increase in PCD compared with normal control. Moreover, no significant difference in the mean plasma VCAM-1 levels was observed when comparing GCD with either PCD or with normal control. Poor glycemic control and increased glucose levels may be responsible for the significantly higher levels of VCAM-1 in PCD. Hyperglycemia leads to increased production of AGE which stimulates vascular inflammation and VCAM-1 expression. This may explain the significant elevation of VCAM-1 in PCD but not in GCD. The sRAGE, which is important in the capture of AGE and prevents the effect of AGE on signaling and alteration of cellular properties, was significantly decreased in PCD but not in GCD. This may emphasize the hypothesis that increased AGE levels in PCD cause elevation of VCAM-1. It is worth mentioning here that an inverse correlation between sRAGE and VCAM-1 was found in the present study. The current study revealed that there was no significant difference in plasma NOx levels in GCD and PCD compared with either normal control or with each other. No change in SOD activities was found in diabetic groups compared with normal controls which may protect NO• from the deleterious O2•– and so, NOx level in diabetic patients didn't differ from that of normal subjects. The present work revealed that there was no significant difference in plasma ox-LDL levels in GCD and PCD compared with either normal control or with each other. Concomitant elevation of circulating glucose and ox-LDL levels is not usually found in well-controlled DM patients, but can be seen in uncontrolled T2DM patients or in some stress conditions, such as in inflammation or infection and during hospitalization. Thus, the exclusion of conditions of inflammation or infection in patients of the present study may explain the unchanged ox-LDL levels. Another explanation for the unchanged ox-LDL levels in diabetic patients in the present study may be the treatment with sulfonylurea, insulin and/or metformin which have antioxidant effects. The present results showed that there was no significant difference in blood SOD activity in GCD and PCD compared with either normal control or with each other. It is possible that changes in SOD activity may occur in early stages of diabetes. Patients in the present study had had diabetes for a long time and had been on long-standing hypoglycemic agents which may be a possible explanation for the unchanged SOD activity in these patients. The current study revealed that there was a significant decrease in blood GSH levels in GCD and PCD compared with normal control. Decreased GSH levels in patients with diabetes may be caused by different pathways including: increased activity of sorbitol pathway which depletes NADPH, and so limits the reduction of GSSG to GSH; decreased activity of glucose-6-phosphate dehydrogenase in hexose monophosphate shunt in DM which generates NADPH; and finally passage of GSSG via erythrocyte membrane which inhibits its reduction to GSH. Another cause for the lower GSH levels in diabetes may be the decreased amino acids necessary for GSH synthesis: L-cysteine, L-glutamate and L-glycine. From this study we can conclude that improvement of glycemic control increases sRAGE and decreases VCAM-1 levels, thus inhibiting the deleterious cascade that results from activation of AGE/RAGE axis. Also, the use of certain hypoglycemic drugs with antioxidant properties in treatment of type 2 diabetes may provide benefit via reduction of oxidative stress. Further studies are needed to investigate whether sRAGE levels are a reproducible and predictive biomarker for the development of diabetic vascular complications. Also, further investigations are needed for the development of strategies aiming at raising sRAGE levels.

PHD Abstract PDF

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