Basic Informations
C.V
CURRICULUM VITAE
Walaa Mohamed Sayed Ahmed
walaa_msa@yahoo.com
Department of clinical pathology
Faculty of Veterinary Medicine,
Beni-Suef university, Egypt
Tel Fax :- +2 082 2327982
Personal Data:-
Date of birth:- 18/11/1978
Nationality:- Egyptian
Gender:- Female
Marital status:- Single
Educational background:
Ph.D:- May 2010 in the field of Veterinary Medicine (Clinical Pathology),
Dissertation : clinicopathological studies on the effect of some
antioxidants against carbon tetrachloride induced toxicity in rat.
M.Sc.: August 2005 in the field of Veterinary Medicine (Clinical Pathology)
Faculty of Veterinary Medicine, CAIRO University, Beni-Suef branch,
Egypt. Dissertation: Clinicopathological studies on experimentally
infected rabbits with bovine herpesvirus – 1
B.Sc.:- 2001 in Veterinary medicine, Faculty of Veterinary medicine, CAIRO
university, Beni-Suef Branch, Egypt.(Grade: very good, Rank: First).
Diploma in Microbiology and Immunology. Faculty of Veterinary
Medicine, Beni-Suef University May 2013.
Employment History
June 2010 to present:-
Lecturer in the department of clinical pathology, Faculty of Veterinary Medicine, Beni-Suef University, Beni-Suef 62511, EGYPT.
Oct. 2007-Oct. 2009:-
Visiting researcher at Laboratory of veterinary Clinical pathobiology, post graduated school of agriculture and life science, The University of Tokyo. Japan.
2005 to 2010:-
Assistant Lecturer in the department of clinical pathology, Faculty of Veterinary Medicine, Cairo University, Beni-Suef branch, Beni-Suef 62511, EGYPT.
2002 to 2005
Demonstrator of Clinical Pathology, department of clinical pathology, Faculty of Veterinary Medicine, Cairo University, Beni-Suef branch, Beni-Suef 62511, EGYPT.
Honors
- Ph. D Scholarship from October 2007 to October 2009 as a governmental
scholarship awarded from The Ministry of Higher Education of Egypt to study in
Japan at The University of Tokyo, Graduated school of agriculture and life
science.
Professional Affiliations:-
Member of the Japanese society of veterinary clinical pathology (JSVCP).
Academic activities:
Teaching undergraduates students from 2002 till now many courses including the following topics:
-outline of clinical pathology
-Different types of samples
-Routine blood examination
-Renal function tests
-Hepatic function tests
-Lipid profile
-Electrophoresis
-Chemical and microscopical urine examination.
Skills and Techniques:-
Biochemistry analysis of body fluid
Cell culture
Tissue slicing
Western blot and oxyblot tech.
Master Title
Clinicopathological studies on experimentally infected rabbits with bovine herpesvirus - 1 (BHV-1)
Master Abstract
Summary
Bovine herpesvirus 1 (BHV-1) is associated with several diseases in cattle namely infectious bovine rhinotracheitis (IBR), infectious pustular vulvovaginitis and infectious balanoposthitis. The incubation period for the respiratory and genital forms is 2-6 days. In the respiratory form the clinical signs range from mild to severe, depending on the presence of secondary bacterial pneumonia. It include pyrexia, anorexia, coughing, excessive salivation, nasal discharge that progresses from serous to mucopurulent, conjunctivitis with lacrimal discharge, and inflamed nares (hence the common name “red nose”). It also cause abortion and reproductive disorders. Such wide variety of clinical syndromes of BHV-1 infection lead to serious economic losses in cattle breeding all over the world.
The present work was carried out to study the effect of BHV-1 on the hemogram, serum biochemical parameters, serological tests and pathological changes of different organs in rabbits.
Forty-eight New-Zealand rabbits of 2-3 months old weighting from 2-3 kg were used. The animals were divided into two main groups, the first group served as control. Rabbits of the second group received 1 ml containing 1 x 107 tissue culture infective dose (TCID) by the intraperitoneal route.
Blood and tissue samples were taken 3,7,10,14, 21, and 28 days post infection for determination of hemogram, some biochemical analysis, electrophoretic pattern of serum proteins, serological tests and histopathological examination.
Results revealed that rabbits infected with BHV-1 showed fever and conjunctivitis. The erythrogram showed no alteration while the leucogram revealed leucocytosis mediated by neutrophilia.
Assay of serum parameters showed significant increase of ALT, AST and AP during the experimental period. Values of BUN and creatinine were elevated throughout the experimental period. Total protein revealed increased value at the 7th day post infection till the end of the experiment. ß – globulin increased at the 3rd and 4th weeks post infection. a- globulin showed elevated values from the 10th day and the 2nd week post infection, while ?- globulin showed elevated values from the 10th day till the end of the experiment. A/G ratio showed significant decrease in the 10th days, and the 2nd and 4th weeks post infection. Study of sodium and potassium values revealed no changes.
Pathological findings of the liver showed degenerative changes, dilatation and congestion of central veins with hyperplastic activation in the Kupffer cells. The lung showed interstitial pneumonia at the 3rd and 4th weeks post infection with emphysema. Trachea showed degenerative changes with hyperplasia of goblet cells. The submucosal blood vessels were dilated and congested accompanied with oedematous changes and leucocytic infiltration at the 10th day post infection till the end of the experiment. Kidney showed degenerative changes of epithelial lining of the renal tubules. Oedema of Bowman’s capsule was obvious in most cases. The spleen showed hyperplasia of lymphoid follicles and widening of sinusoids of red pulp. Microscopic examination of adrenal glands of all animals revealed a progressive degranulation and vacuolation of chromaffin cells of the medulla.
Evaluation of humoral immune response against infection revealed increase of antibody titer from the first week of infection till the end of the experiment with a peak at the third week of the experiment.
PHD Title
Clinicopathological studies on the protective effect of some antioxidants against carbon tetrachloride-induced toxicity in rats
PHD Abstract
Summary and Conclusion
Clinical evidence has shown that liver is a target organ for carbon tetrachloride toxicity. The aim of the present in vitro study was to: (1) evaluate the hepatotoxic effect of CCL4 using hepatocytes cell line (BRL3A)and (2) investigate the possible protective effects of antioxidants, namely ascorbic acid , mannitol and aminoguanidine against carbon tetrachloride induced cytotoxicity and oxidative stress comparable with vitamin E as standard hepatoprotective agent. Hepatocytes cell line was incubated with 7.5 µl of pure CCL4. To evaluate the potential protective effect of antioxidants, cells were incubated with vitamin E in the final concentrations of 100, 50, 25 and 12.5 µM or ascorbic acid in the final concentrations of 500, 250, 125 and 62.5 µM or mannitol in the final concentrations of 400, 200 and 100 µM (low doses), 20 mM and 10 mM (high doses) and aminoguanidine in the final concentrations of 400, 200 and 100 µM. The toxic effect of CCL4 was evaluated by measuring the generated free radicals, the leakage of LDH, ALT and AST enzymes, the formation of TBARS, carbonyl proteins and detection of apoptotic cells by TUNEL method. Results of this experiment showed that treatment with vitamin E improved the cell viability as compared with CCL4 treated group, as manifested with reduction in the leakage of LDH, ALT and AST enzymes, reduction of the oxidative DNA damage, and oxidation of protein generated by CCL4 toxicity (dose dependent). Ascorbic acid was able only to reduce the LDH leakage at 500 µM after 24 hr. Mannitol neither reduce the leakage of enzymes, nor the extent of oxidative DNA damage and oxidation of proteins. Aminoguanidine was ineffective against CCL4 induced toxicity in cell culture, and it exhibited pro-oxidant properties.
In conclusion:-
The present study indicate that CCL4 has a potential cytotoxic effect in BRL3A cell culture. There was no evidence of CCL4 -initiated lipid peroxidation detected in this study. In addition, apoptosis represents one of the mechanisms of cell death after CCL4- induced liver injury.
Vitamin E seems more effective and provide complete protection against CCL4 induced hepatotoxicity in culture cells. Ascorbic acid, mannitol and aminoguanidine were ineffective against CCL4 toxicity.
Aminoguanidine may act as antioxidant in vivo but in vitro it generates H2O2, so it has pro-oxidant activity.