Monday, October 29, 2012

BibTeX for Dr ehab aboueladab


@article{brandt2008galectin,
  title={Galectin-1 induced activation of the apoptotic death-receptor pathway in human Jurkat T lymphocytes},
  author={Brandt, B. and B{\"u}chse, T. and Abou-Eladab, E.F. and Tiedge, M. and Krause, E. and Jeschke, U. and Walzel, H.},
  journal={Histochemistry and cell biology},
  volume={129},
  number={5},
  pages={599--609},
  year={2008},
  publisher={Springer}
}

@article{walzel2006effects,
  title={Effects of N-glycan processing inhibitors on signaling events and induction of apoptosis in galectin-1-stimulated Jurkat T lymphocytes},
  author={Walzel, H. and Fahmi, A.A. and Eldesouky, M.A. and Abou-Eladab, E.F. and Waitz, G. and Brock, J. and Tiedge, M.},
  journal={Glycobiology},
  volume={16},
  number={12},
  pages={1262--1271},
  year={2006},
  publisher={Soc Glycobiology}
}

@article{brandt2010role,
  title={Role of the JNK/c-Jun/AP-1 signaling pathway in galectin-1-induced T-cell death},
  author={Brandt, B. and Abou-Eladab, EF and Tiedge, M. and Walzel, H.},
  journal={Cell death \& disease},
  volume={1},
  number={2},
  pages={e23},
  year={2010},
  publisher={Nature Publishing Group}
}

@article{jagannadham2011identification,
  title={Identification of outer membrane proteins from an Antarctic bacterium Pseudomonas syringae Lz4W},
  author={Jagannadham, M.V. and Abou-Eladab, E.F. and Kulkarni, H.M.},
  journal={Molecular \& Cellular Proteomics},
  volume={10},
  number={6},
  year={2011},
  publisher={ASBMB}
}

@article{abdel1996buffalo,
  title={Buffalo (< i> Bos Buffali L.</i>) chymosin purification and properties},
  author={Abdel Malak, C.A. and Abou El Adab, I.F.G. and Vukashinovic, V. and Zalunin, I.A. and Timokhina, E.A. and Lavrenova, G.I. and Stepanov, V.M.},
  journal={Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology},
  volume={113},
  number={1},
  pages={57--62},
  year={1996},
  publisher={Elsevier}
}

@article{abouevaluation,
  title={Evaluation of protein preparations from bacteria using proteomics approaches: Application to an Antarctic bacterium Pseudomonas syringae},
  author={Abou-Eladab, E.F. and Idris, M.M. and Jagannadham, M.V.}
}



------------------------------------------ Best Wishes: Dr.Ehab Aboueladab, Tel:01007834123 Email:ehab10f@gmail.com,ehababoueladab@yahoo.com ------------------------------------------

EndNote -publication Dr ehab aboueladab


%0 Journal Article
%T Galectin-1 induced activation of the apoptotic death-receptor pathway in human Jurkat T lymphocytes
%A Brandt, B.
%A B├╝chse, T.
%A Abou-Eladab, E.F.
%A Tiedge, M.
%A Krause, E.
%A Jeschke, U.
%A Walzel, H.
%J Histochemistry and cell biology
%V 129
%N 5
%P 599-609
%@ 0948-6143
%D 2008
%I Springer


%0 Journal Article
%T Effects of N-glycan processing inhibitors on signaling events and induction of apoptosis in galectin-1-stimulated Jurkat T lymphocytes
%A Walzel, H.
%A Fahmi, A.A.
%A Eldesouky, M.A.
%A Abou-Eladab, E.F.
%A Waitz, G.
%A Brock, J.
%A Tiedge, M.
%J Glycobiology
%V 16
%N 12
%P 1262-1271
%@ 0959-6658
%D 2006
%I Soc Glycobiology


%0 Journal Article
%T Role of the JNK/c-Jun/AP-1 signaling pathway in galectin-1-induced T-cell death
%A Brandt, B.
%A Abou-Eladab, EF
%A Tiedge, M.
%A Walzel, H.
%J Cell death & disease
%V 1
%N 2
%P e23
%D 2010
%I Nature Publishing Group


%0 Journal Article
%T Identification of outer membrane proteins from an Antarctic bacterium Pseudomonas syringae Lz4W
%A Jagannadham, M.V.
%A Abou-Eladab, E.F.
%A Kulkarni, H.M.
%J Molecular & Cellular Proteomics
%V 10
%N 6
%@ 1535-9476
%D 2011
%I ASBMB


%0 Journal Article
%T Buffalo (< i> Bos Buffali L.</i>) chymosin purification and properties
%A Abdel Malak, C.A.
%A Abou El Adab, I.F.G.
%A Vukashinovic, V.
%A Zalunin, I.A.
%A Timokhina, E.A.
%A Lavrenova, G.I.
%A Stepanov, V.M.
%J Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology
%V 113
%N 1
%P 57-62
%@ 1096-4959
%D 1996
%I Elsevier


%0 Journal Article
%T Evaluation of protein preparations from bacteria using proteomics approaches: Application to an Antarctic bacterium Pseudomonas syringae
%A Abou-Eladab, E.F.
%A Idris, M.M.
%A Jagannadham, M.V.



------------------------------------------ Best Wishes: Dr.Ehab Aboueladab, Tel:01007834123 Email:ehab10f@gmail.com,ehababoueladab@yahoo.com ------------------------------------------

publication dr ehab aboueladab


TY  - JOUR
T1  - Galectin-1 induced activation of the apoptotic death-receptor pathway in human Jurkat T lymphocytes
A1  - Brandt, B.
A1  - B├╝chse, T.
A1  - Abou-Eladab, E.F.
A1  - Tiedge, M.
A1  - Krause, E.
A1  - Jeschke, U.
A1  - Walzel, H.
JO  - Histochemistry and cell biology
VL  - 129
IS  - 5
SP  - 599
EP  - 609
SN  - 0948-6143
Y1  - 2008
PB  - Springer
ER  -


TY  - JOUR
T1  - Effects of N-glycan processing inhibitors on signaling events and induction of apoptosis in galectin-1-stimulated Jurkat T lymphocytes
A1  - Walzel, H.
A1  - Fahmi, A.A.
A1  - Eldesouky, M.A.
A1  - Abou-Eladab, E.F.
A1  - Waitz, G.
A1  - Brock, J.
A1  - Tiedge, M.
JO  - Glycobiology
VL  - 16
IS  - 12
SP  - 1262
EP  - 1271
SN  - 0959-6658
Y1  - 2006
PB  - Soc Glycobiology
ER  -


TY  - JOUR
T1  - Role of the JNK/c-Jun/AP-1 signaling pathway in galectin-1-induced T-cell death
A1  - Brandt, B.
A1  - Abou-Eladab, EF
A1  - Tiedge, M.
A1  - Walzel, H.
JO  - Cell death & disease
VL  - 1
IS  - 2
SP  - e23
Y1  - 2010
PB  - Nature Publishing Group
ER  -


TY  - JOUR
T1  - Identification of outer membrane proteins from an Antarctic bacterium Pseudomonas syringae Lz4W
A1  - Jagannadham, M.V.
A1  - Abou-Eladab, E.F.
A1  - Kulkarni, H.M.
JO  - Molecular & Cellular Proteomics
VL  - 10
IS  - 6
SN  - 1535-9476
Y1  - 2011
PB  - ASBMB
ER  -


TY  - JOUR
T1  - Buffalo (< i> Bos Buffali L.</i>) chymosin purification and properties
A1  - Abdel Malak, C.A.
A1  - Abou El Adab, I.F.G.
A1  - Vukashinovic, V.
A1  - Zalunin, I.A.
A1  - Timokhina, E.A.
A1  - Lavrenova, G.I.
A1  - Stepanov, V.M.
JO  - Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology
VL  - 113
IS  - 1
SP  - 57
EP  - 62
SN  - 1096-4959
Y1  - 1996
PB  - Elsevier
ER  -


TY  - JOUR
T1  - Evaluation of protein preparations from bacteria using proteomics approaches: Application to an Antarctic bacterium Pseudomonas syringae
A1  - Abou-Eladab, E.F.
A1  - Idris, M.M.
A1  - Jagannadham, M.V.
ER  -



------------------------------------------ Best Wishes: Dr.Ehab Aboueladab, Tel:01007834123 Email:ehab10f@gmail.com,ehababoueladab@yahoo.com ------------------------------------------

E=mc² is Incomplete



------------------------------------------Best Wishes: Dr.Ehab Aboueladab, Tel:01007834123 Email:ehab10f@gmail.com,ehababoueladab@yahoo.com ------------------------------------------

Sunday, October 28, 2012

الوطن | الكساد يضرب دمياط ليلة "الأضحى"..والمواطنون عصر "مرسي" أسوأ من "مبارك"

الوطن | الكساد يضرب دمياط ليلة "الأضحى"..والمواطنون عصر "مرسي" أسوأ من "مبارك"

------------------------------------------Best Wishes: Dr.Ehab Aboueladab, Tel:01007834123 Email:ehab10f@gmail.com,ehababoueladab@yahoo.com ------------------------------------------

نهر الأمازون يقع في أمريكا الجنوبية


 نهر الأمازون يقع في أمريكا الجنوبية. وهو أكبر نهر في العالم من حيث الحجم والعمق، ومن حيث معدل التدفق الذي يفوق معدل تدفق أكبر ثماني أنهار في العالم الذين يلونه في الترتيب مجتمعين.
يزداد اتساع أجزاء من الأمازون عن 190 كيلومتر (120 ميل) أثناء موسم الأمطار. ونظرا لاتساعه يطلق عليه أحيانا البحر النهر.
في حين أن نهر الأمازون هو أغزر نهر في العالم، إلا أن البيانات الحالية للجمعية الجغرافية تشير إلى أن الأمازون هو ثاني أطول نهر في العالم بعد نهر النيل. ومع ذلك يجادل بعض العلماء خاصة من البرازيل وبيرو بخصوص ذلك.






















------------------------------------------ Best Wishes: Dr.Ehab Aboueladab, Tel:01007834123 Email:ehab10f@gmail.com,ehababoueladab@yahoo.com ------------------------------------------

Diabetes Mellitus


Q.1- What is the biochemical basis for the followings in Diabetes Mellitus-
a) Weight loss
b) Paresthesias
c) Increased susceptibility to infections
d) Non healing ulcers
e) Blindness
f) Hypoglycemia
g) Lactic acidosis
h) Ketosis
i) Hypercholesterolemia
j) High risk for IHD
Q- 2 What is Glycated hemoglobin? What is its significance in the diagnosis of Diabetes mellitus?
Q.3- What is the cause of Hypokalemia upon insulin administration in diabetics?
Q.4.- What is Maturity onset diabetes mellitus of young (MODY)?
Q.5-What is LADA (Latent Auto immune diabetes mellitus of Adults)?
Q.6- What are the important differences between Type1 and Type 2 diabetes mellitus?
Q.7- What is the cause of insulin resistance in type 2 diabetes mellitus?
Q.8-A 35 year- old woman reported with classical symptoms of polyuria, Polyphagia and Polydipsia. Her fasting blood glucose was 190 mg/dl. She was diagnosed witDiabetes mellitus and was started with oral hypoglycemic drugs. A week laterher blood glucose was repeated and was found to be 234 mg/dl.  What could be the reason for increasing blood glucose level despite glucose lowering therapy? Which investigation should bcarried out for further diagnosis?
Q.9-What is the significance of estimating c-peptide levels?
Q.10- What are diabetes prone states?
Q.11-What are the secondary causes of diabetes mellitus?
Q.12- What is the significance of detecting microalbuminuria in diabetes mellitus?
Q.13-What is the biochemical basis for impaired glucose uptake inskeletal muscles and adipose tissue in diabetes mellitus?
Q.14- What is the biochemical basis for complications in diabetes mellitus?
Q.15- What are the acute complications of diabetes mellitus?
Q.16-What are late onsets or chronic complications of diabetes mellitus?
Q.17-What is meant by “Advanced glycation end products”?
Q.18- What are the metabolic alterations brought about in the absence of insulin in diabetes mellitus?
Q.19- Enumerate the different tests carried out for the diagnosis of diabetes mellitus?
Q.20 Suggest a healthy diet for a diabetic patient? What is the role of dietary fiber?
Q.21- What is the treatment for diabetic ketoacidosis?
Q.22- What should be the fasting and post load blood glucose values for a person to be declared as  having impaired glucose tolerance?
Q.23- What are the indication for carrying out oral glucose tolerance test ?
Q.24 -What is the criteria for the laboratory diagnosis of diabetes mellitus after oral glucose tolerance test?
Q.25- What is the significance of serum fructosamine estimation in diabetes mellitus?



----------------------------------------- Best Wishes: Dr.Ehab Aboueladab, Tel:01007834123 Email:ehab10f@gmail.com,ehababoueladab@yahoo.com ------------------------------------------

patient is suffering from Diabetes Insipidus

A 23-year-old male was seen in the emergency department after suffering a concussion and head trauma from a motor vehicle accident. The patient was stabilized in the emergency department and transferred to the intensive care unit (ICU) for observation. The patient had computed tomography(CT) scan of the head that revealed a small amount of cerebral edema but was otherwise normal. During the second day in the ICU, the nurse informed that the patient had a large amount of urine output in the last 24 hours. The nursing records reported his urine output over the previous 24 hours to be 5000 cc. He had not been given any diuretic medications. A urine osmolality was ordered and was found to be low. His physician remarked that the kidneys were not concentrating urine normally.

What is the most likely diagnosis for the increasing dilute urine output?
Which biochemical mediator is responsible for this disorder ?
Case details The patient is suffering from Diabetes Insipidus.  Excessive excretion of diluted urine with a low osmolarity and history of head injury are all suggestive of diabetes Insipidus. Head trauma is one of the most common causes of diabetes Insipidus, particularly if the posterior pituitary stalk is disrupted. 
Polyuria, Polydipsia,high plasma osmolarity and a low urinary osmolarity are hall marks of diabetes Insipidus. Diabetes Insipidus is not the same as diabetes mellitus (“sugar” diabetes).  Diabetes Insipidus resembles diabetes mellitus because the symptoms of both diseases are increased urination and thirst.  However, in every other respect, including the causes and treatment of the disorders, the diseases are completely unrelated.   Sometimes diabetes Insipidus is referred to as”water” diabetes to distinguish it from the more common diabetes mellitus or “sugar” diabetes.

Pathophysiology           
The regulation of urine production occur in the hypothalamus, which produces ADH in the supraoptic and Para ventricularnuclei. After synthesis, the hormone is transported in neuro secretory granules down the axon of the hypothalamic neuron to the posterior lobe of the pituitargland where it is stored for later release. In addition, the hypothalamus regulates the sensation of thirst in the ventromedial nucleus by sensing increases in serum osmolarity and relaying this information to the cortex.
The main effector organ for fluid homeostasis is the kidney. ADH acts by increasing water permeability in the collecting ducts and distal convoluted tubule, specifically it acts on proteinscalled aquaporins which open to allow water into the collecting duct cells.This increase in permeability allows for reabsorption of water into the bloodstream, thus concentrating the urine.
Signs and symptoms
Excessive urination and extreme thirst are typical for DI. Symptoms of diabetes Insipidus are quite similar to those of untreated diabetes mellitus, with the distinction that the urine does not contain glucose and there is no hyperglycemia. Signs of dehydration may also appear in some individuals since the body cannot conserve much of the water it takes in.
The extreme urination continues throughout the day and the night. In children, DI can interfere with appetite, eating,weight gain, and growth as well. They may present with fever, vomiting, ordiarrhea. Adults with untreated DI may remain healthy for decades as long as enough water is consumed to off set the urinary losses. However, there is a continuous risk of dehydration and loss of potassium.
Biochemical defect -Diabetes Insipidus is divided into four types, each of which has a different cause and must be treated differently. 
1) Central or neurogenic DI- The most common type of DI is caused by a lack of vasopressin, a hormone that normally acts upon the kidney to reduce urine output by increasing the concentration of the urine.  This type of DI isusually due to the destruction of the “posterior” part of the pituitary gland where vasopressin is normally produced.  Hence, it is commonly called pituitaryDI.   
The posterior pituitary can be destroyed by a variety of underlying diseases including tumors, infections, head injuries(As in the given patient), infiltrations, and various inheritable defects. The latter can be recognized by the onset of the DI in early childhood and a family history of parents, siblings or other relatives with the same disorder.  Nearly half the time, however, pituitary DI is”idiopathic” (that is, no cause can be found despite a thorough search including magnetic resonance imaging or MRI of the brain) and the underlying cause(s) is (are) still unknown.  
2) Gestagenic or gestational DI -Occasionally,a lack of vasopressin can also develop during pregnancy if the pituitary is slightly damaged and/or the placenta destroys the hormone too rapidly. 
3) Nephrogenic DI -The third type of DI is caused by an inability of the kidneys to respond to the “antidiuretic effect” of normal amounts of vasopressin.  The kidneys’ ability to respond to ADH can be impaired bydrugs—like lithium, for example—and by chronic disorders including polycystic kidney disease, sickle-cell disease, kidney failure, partial blockage of the ureters, and inherited genetic disorders.
4) DipsogenicDI -The fourth form of DI occurs when vasopressin is suppressed by excessive intake of fluids.  The latter is usually referred to as primary polydipsia and is most often caused by an abnormality in the part of the brain that regulates thirst.  This subtype is difficult to differentiate from pituitary DI particularly since the two disorders can result form  many of the same brain diseases. 
Diagnosis
Diagnosis is based on a series of tests,including urinalysis and a fluid deprivation test.
Urine analysis -The urine of a person with DI will be less concentrated.
A fluid deprivation test helps determine whether DI is caused by one of the following:

  • excessive intake of fluid
  • a defect in ADH production
  • a defect in the kidneys’ response to ADH
This test measures changes in body weight,urine output, and urine composition when fluids are withheld. Sometimes measuring blood levels of ADH during this test is also necessary.
Desmopressin stimulation Test -To distinguish between the main forms,desmopressin stimulation is also used; desmopressin can be taken by injection,a nasal spray, or a tablet. While taking desmopressin, a patient should drink fluids or water only when thirsty and not at other times, as this can lead to sudden fluid accumulation in the central nervous system. If desmopressin reduces urine output and increases osmolarity, the pituitary production of ADH is deficient, and the kidney responds normally. If the DI is due to renal pathology, desmopressin does not change either urine output or osmolarity.
In order to distinguish DI from other causes of excess urination, blood glucose levels, bicarbonate levels, and calcium levels need to be tested. Measurement of blood electrolytes can reveal a high sodium level (hypernatremia as dehydration develops).
In some patients, a magnetic resonance imaging (MRI) of the brain may be necessary as well.
Treatment
Central DI and gestational DI respond todesmopressin, a synthetic analogue of ADH. Gestational DI tends to abate on itsown 4 to 6 weeks following labor, though some women may develop it again in subsequent pregnancies. In dipsogenic DI, desmopressin is not usually an option.
Desmopressin is ineffective in nephrogenic DI. 
Again, adequate hydration is important for patients with DI, as they may become dehydrated easily.


------------------------------------------ Best Wishes: Dr.Ehab Aboueladab, Tel:01007834123 Email:ehab10f@gmail.com,ehababoueladab@yahoo.com ------------------------------------------

Hypercalcemia


A 35 year -oid female reported to emergency with severe pain in the left flank region, which was radiating towards lower leg and back. The patient was in acute distress and agony. History revealed that she frequently suffered from urinary tract infections and had several such episodes of pain.She further reported that she constantly felt weakness, fatigue and bone pains from the previous few months. There was no history of fever and there was no personal or family history of medical problems.
Her physical examination was normal except for tenderness in the left renal region.
The attending physician ordered for complete blood count, electrolytes and a complete urinalysis.
The laboratory investigation report revealed a normal complete blood count (CBC), and significantly elevated calcium level and low phosphorus level. Urine was cloudy and had plenty of pus cells. The patient was admitted and treated for renal colic.
What is the underlying cause for repeated episodes of renal colic?
What is the most likely diagnosis?
What is the relationship of bone pains and frequent urinary tract infections in this patient?
What is the cause for high serum calcium and low phosphorus level in this patient?



------------------------------------------ Best Wishes: Dr.Ehab Aboueladab, Tel:01007834123 Email:ehab10f@gmail.com,ehababoueladab@yahoo.com ------------------------------------------

Hypercalcemia


A 35 year -oid female reported to emergency with severe pain in the left flank region, which was radiating towards lower leg and back. The patient was in acute distress and agony. History revealed that she frequently suffered from urinary tract infections and had several such episodes of pain. She further reported that she constantly felt weakness, fatigue and bone pains from the previous few months.
There was no history of fever and there was no personal or family history of medical problems.
Her physical examination was normal except for tenderness in the left renal region.The attending physician ordered for complete blood count, electrolytes and a complete urinalysis.
The laboratory investigation report revealed a normal complete blood count (CBC), and significantly elevated calcium level and low phosphorus level.Urine was cloudy and had plenty of pus cells. The patient was admitted and treated for renal colic.
What is the underlying cause for repeated episodes of renal colic?
What is the most likely diagnosis?
What is the relationship of bone pains and frequent urinary tract infections in this patient?
What is the cause for high serum calcium and low phosphorus level in this patient?

Case details Hypercalcemia, hypophosphatemia, recurrent urinary tract infections, renal stones and bone pains all signify underlying hyperparathyroidism. (Cloudy urine and pus cells are indicative of urinary tract infection).
Hyperparathyroidism is over activity of the parathyroid glands resulting in excess production of parathyroid hormone (PTH). The parathyroid hormone regulates calcium and phosphate levels.  
Hyperparathyroidism is classified in three categories-
1) Primary hyperparathyroidism-Primary hyperparathyroidism results from a hyper function of the parathyroid glands themselves. There is over secretion of PTH due to adenoma, hyperplasia or,rarely, carcinoma of the parathyroid glands.
2) Secondary hyperparathyroidism-Secondary hyperparathyroidism is the reaction of the parathyroid glands to a hypocalcaemia caused by something other than a parathyroid pathology, e.g.chronic renal failure or vitamin D deficiency.
3)Tertiary hyperparathyroidism- Tertiary hyperparathyroidism results from hyperplasia of the parathyroid glands and a loss of response to serum calcium levels. In cases of long-standing secondary hyperparathyroidism, the hypertrophied parathyroid glands can become autonomously functioning and continue to secrete PTH independent of whether the original stimuli to secrete PTH are still present.
In all cases, the raised PTH levels are harmful to bone, and treatment is often needed.
Serum calcium- In cases of primary hyperparathyroidism or tertiary hyperparathyroidism heightened PTH leads to increased serum calcium (Hypercalcemia) due to:
  1. increased bone resorption, allowing flow of calcium from bone to blood
  2. reduced renal clearance of calcium
  3. increased intestinal calcium absorption
By contrast, in secondary hyperparathyroidism effectiveness of PTH is reduced.
Serum phosphate
In primary hyperparathyroidism, serum phosphate levels are abnormally low as a result of decreased renal tubular phosphate reabsorption. However, this is only present in about 50% of cases.This contrasts with secondary hyperparathyroidism, in which serum phosphate levels are generally elevated because of renal disease.
Manifestations of hyperparathyroidism involve primarily the kidneys and the skeletal system. Kidney involvement is due to either deposition of calcium in the renal parenchyma or to recurrent nephrolithiasis. Renal stones are usually composed of either calcium oxalate or calcium phosphate. In occasional patients,repeated episodes of nephrolithiasis or the formation of large calculi may lead to urinary tract obstruction, infection, and loss of renal function. 
Nephrocalcinosis may also cause decreased renal function and phosphate retention.
There are great variations in the manifestations. Patients may present with multiple signs and symptoms, including recurrent nephrolithiasis, peptic ulcers,mental changes, and, less frequently, extensive bone resorption.
Treatment and monitoring Treatment depends upon the severity and cause of the condition. If there is mildly increased calcium levels due to primary hyperparathyroidism and no symptoms, just regular check ups are needed. If symptoms are present or calcium level is very high, surgery may be needed to remove the parathyroid gland that is overproducing the hormone. Treatment of secondary hyperparathyroidism depends on the underlying cause.Vitamin D and Phosphorus supplementation can also be done. 
Calcimimetics
A Calcimimetics (cinacalcet) is a new type of drug for people with primary and secondary hyperparathyroidism on dialysis. It mimics the effect of calcium in tissues. This reduces PTH release from parathyroid glands, leading to lower calcium and phosphorus levels in blood. 
Surgery for hyperparathyroidism may lead to low blood calcium levels, which causes tingling and muscle twitching. This requires immediate treatment.



------------------------------------------ Best Wishes: Dr.Ehab Aboueladab, Tel:01007834123 Email:ehab10f@gmail.com,ehababoueladab@yahoo.com ------------------------------------------