Search In this Thesis
   Search In this Thesis  
العنوان
Assessment of Estrogen Receptor Beta Polymorphisms in Male Patients with Unexplained Infertility /
المؤلف
Hemdan,Islam Sobhy Ahmed
هيئة الاعداد
باحث / اسلام صبحي احمد حمدان
مشرف / رشاد محمود مصطفي
مشرف / حليم ماهر حليم
مشرف / هدي يسري عبدالله
الموضوع
Dermatology and Venereology.
تاريخ النشر
2021
عدد الصفحات
130 P. ;
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الأمراض الجلدية
تاريخ الإجازة
1/1/2021
مكان الإجازة
جامعة قناة السويس - كلية الطب - Dermatology and Venereology
الفهرس
Only 14 pages are availabe for public view

from 151

from 151

Abstract

Infertility has become a common problem as it is affecting almost 1 in 6 couples. It is defined as the incapability to achieve fertilization after a certain period of time following sexual intercourse (mostly 1 year or 6 months in certain cases) without any contraceptive measures. Infertility cannot be associated with a specific gender as both male and female factors account for 40 % while 20 % cases are either due to shared or unexplained causes.
Numerous genes are involved in the complex process of reproduction. A qualitative diagnosis of infertility could only be done by focusing on female and male physical abnormalities, endocrine irregularities and genetic conditions of both partners associated with reproduction.
Male infertility is an important cause of couple’s inability to bear children in 20% to 25% of total cases and the etiology of nearly half of the cases remains idiopathic. Approximately 15% of male infertile cases, genetic factors, including chromosomal aberrations and single gene mutations, may result in spermatogenic failure and sperm dysfunction.
The traditional view of estradiol as the ‘female’ hormone and of testosterone as the ‘male’ hormone has been challenged due to the increased interest in elucidating the role of estrogen in males. Estrogens are produced in the male reproductive system by Sertoli cells, Leydig cells, and germ cells.
In addition, studies revealed that estrogens reduce testosterone production from Leydig cells and reduce Sertoli cell numbers in adult when they are given during development. The estrogens can also disrupt fetal Leydig cell development, inhibit apoptosis of human postmeiotic