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العنوان
The Value Of Pregnancy Sppecific B1 Glycoprottein (SP1) In Maternal Serum For The Diagnosis Of Intauterine Growth Retardation ( Iugr) In Pre- Eclampticc Toxaemmia =
الناشر
Alex uni F.O.Medicine ,
المؤلف
Yousef, Mohamed Mohameed Hafez .
هيئة الاعداد
باحث / محمد محمد حافظ يوسف
مشرف / مختار طوبه زاده
مشرف / منى سدراك
مشرف / ايمان درويش
الموضوع
Obstetrics And Gynaecology .
تاريخ النشر
1988 .
عدد الصفحات
P83. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب
تاريخ الإجازة
1/1/1988
مكان الإجازة
جامعة الاسكندريه - كلية الطب - Obstetrics And Gynaecology
الفهرس
Only 14 pages are availabe for public view

from 87

from 87

Abstract

The pathophysiology of rhino sinusitis is multifactorial. However, regardless of
etiology, the common basis for the development of sinus disease is often associated with
mucous stasis due to ostiomeatal obstruction and/or mucociliary dysfunction. Persistent
obstruction results in decreased oxygen tension, reduced sinus pH, ciliary dysfunction, and
negative pressure within the sinus cavity. Sneezing or nose blowing may cause a transient
opening of the sinus drainage pathways. This, in addition to negative pressure within the
sinus cavity, may result in the inoculation of pathogenic bacteria from the nasal cavity or
nasopharynx into the sinus cavity. (٢٠, ٢١)
An optimal environment for overgrowth is thereby achieved, resulting in rhino
sinusitis. There has been a great interest in identifying pathways for the development of
rhino sinusitis. The inflammatory roles of bacteria and fungi, and the subsequent response
by inflammatory cells and production of mediators of inflammation have generated new
thinking regarding the pathophysiology. A noninfectious inflammatory response as a
result of bacterial or fungal colonization resembling ‘‘allergic or asthmatic’’ inflammation
has been described. The host inflammatory response with production of inflammatory
cytokines may be the underlying cause of rhino sinusitis. Of particular interest in this area
are the role of bacterial, fungal allergy, eosinophilic inflammation, biofilms, and
superantigens. (٢٠, ٢١)