Basic Informations
C.V
1. Personal data:
Mohamed Gamal Hasssan Ali
|
Name:
|
Fayoum
|
Place of birth :
|
25/12/1987
|
Date of birth:
|
Egyptian
|
Nationality :
|
Arabic – English
|
Language :
|
pharmacy
|
General
specialization:
|
Biochemistry and molecular biology
|
Accurate specialization:
|
Mohamedgamal_pharmacy@yahoo.com
|
E-mail:-
|
|
Personal account:
|
2. Scientific qualification:
Country
|
Affiliation
|
Faculty
|
General specification
|
Date
|
Degree
|
Egypt
|
Bani-suef university
|
Faculty of pharmacy
|
pharmacy
|
2010
|
Bachelor of pharmaceutical science
|
|
|
|
|
|
|
|
|
|
|
|
|
- Chronology of Employment:
Country
|
Affiliation
|
The end of employment
|
The start of employment
|
Academic degree
|
Job
|
egypt
|
Faculty of pharmacy bani-suef university
|
|
3/2011
|
Master student
|
Demonstrator of biochemistry
|
|
|
|
|
|
|
|
|
|
|
|
|
4. Courses and workshops:
Year
|
place
|
Nature of course/ workshop
|
Name of course
|
2010
|
Faculty of pharmacy bani-suef university
|
|
C.V writing
|
2010
|
Faculty of pharmacy bani-suef university
|
|
Patient counceing
|
2010
|
Faculty of pharmacy bani-suef university
|
|
Interviewing skills
|
2010
|
Faculty of pharmacy bani-suef university
|
|
Pharmaceutical career path
|
2011
|
bani-suef university
|
|
Advanced word processing
|
2011
|
bani-suef university
|
|
Advanced power point
|
2011
|
bani-suef university
|
|
Advanced database
|
2011
|
bani-suef university
|
|
Advanced spreadsheets
|
2013
|
bani-suef university
|
|
Analysis of literature on redox regulation and redox signaling
|
2013
|
bani-suef university
|
|
Self-marketing
|
2013
|
bani-suef university
|
|
Development of quality systems at faculties of Beni-Suef University
|
7. Academic experiences:
A- Teached courses:
Accurate specialization
|
University
|
Faculty
|
Grade
|
Language
|
Course name
|
Biochemistry and molecular biology
|
Bani-suef
|
Faculty of pharmacy
|
|
English
|
Practical biochemistry I
|
Biochemistry and molecular biology
|
Bani-suef
|
Faculty of pharmacy
|
|
English
|
Practical biochemistry II
|
Biochemistry and molecular biology
|
Bani-suef
|
Faculty of pharmacy
|
|
English
|
Practical biochemistry III
|
Biochemistry and molecular biology
|
Bani-suef
|
Faculty of pharmacy
|
|
English
|
Clinical nutrition
|
Master Title
Role of MAPK pathway in lipopolyssacharide/D-galactosamine induced hepatotoxicity in rats rats
Master Abstract
Administration of D-galactosamine (D-GalN) and lipopolysaccharide (LPS) caused activation of toll like receptor 4 (TLR4) and subsequent activation of NADPH oxidase 4 (NOX4) and therefore increased production of reactive oxygen species (ROS). ROS production caused activation of mitogen activated protein kinase (MAPK) by phosphorylation of apoptosis signal-regulating kinase1 (ASK1) and therefore phosphorylation of P38 MAPK. ROS generation decreased gene expression levels of thioredoxin1 (Trx1), thioredoxin reductase 1 (TrxR1), protein phosphatase 5 (PP5). Therefore our aim was to address the role of D-GalN and LPS on hepatotoxicity in rats through studying the MAPK pathway and to evaluate the effect of silibinin and vitamin E on TrxR1 and PP5 as one of the regulatory mechanisms responsible for hepatocellular protection against D-GalN/LPS induced oxidative stress. Acute rat liver injury was induced by co-administration of D-GalN/LPS. Silibinin and vitamin E were used as a hepatoprotective against this liver injury. Serum ALT and AST, oxidative (MDA) and antioxidant markers (GSH, CAT and SOD) were measured. Expression levels of Trx1, TrxR1, PP5, NOX4, ASK1 and P38 MAPK were determined. Treatment or prophylaxis of either silibinin or vitamin E significantly decreased ALT, AST, MDA, NOX4, ASK1 and P38 MAPK levels and significantly increased GSH, CAT, SOD, Trx1, TrxR1 and PP5 levels when compared with D-GalN/LPS treated group. It can be concluded that administration of D-GalN/LPS caused rat liver injury that was through excess ROS generation which consequently induced activation of MAPK cascade. Silibinin or vitamin E succeeded in ameliorating the deleterious effects of D-GalN/LPS induced oxidative stress.
PHD Title
PHD Abstract