دانلود مقاله Genotyping and phenotyping Helicobacter pylori virulence markers in Iranian gastric cancer and non gastric cancer patients با word دارای 4 صفحه می باشد و دارای تنظیمات در microsoft word می باشد و آماده پرینت یا چاپ است

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توجه : در صورت  مشاهده  بهم ریختگی احتمالی در متون زیر ،دلیل ان کپی کردن این مطالب از داخل فایل ورد می باشد و در فایل اصلی دانلود مقاله Genotyping and phenotyping Helicobacter pylori virulence markers in Iranian gastric cancer and non gastric cancer patients با word،به هیچ وجه بهم ریختگی وجود ندارد

بخشی از متن دانلود مقاله Genotyping and phenotyping Helicobacter pylori virulence markers in Iranian gastric cancer and non gastric cancer patients با word :

سال انتشار: 1384

محل انتشار: چهارمین همایش ملی بیوتکنولوژی ایران

تعداد صفحات: 4

نویسنده(ها):

masoud ghaffarpour – Biotechnology Research Cenyer, Pasteur Institute of Iran
Mohammad Ali Mohagheghi – Cancer Institute, Tehran Medical University
H.R Vaziri – Gastroenterology Department Mofarrah Hospital

چکیده:

The epidemionology of Helicobacter pylori (Hp) infection in Iran creates a public health implication because of its high prevalence and its association woth gastric cancer and peptic ulcer disease. Recent studies suggest that genotypes and phenotypes of Hp in regards to its virulence markers such as VacA and CagA potentially correlate with severity of the associated gastroduodenal diseases. Hp strains possessing vacA gene with signal sequence/middle region combination type s1m1 are identified as highly toxic and are associated with increased gastric epithelial damages, enhanced gastric inflammation and doudenal ulcertion.However, in developing countries, Type I Hp strains (cagA + vacA tox+) are highly prevalent regardless of the clinical manifestations. To evaluate the most prevalent genotype among our highly infected population, Hp strains were isolated from 25 gastric cancer (GC) and 61 non GC patients. Analusis of vacuolating cytotoxin gene (vacA) and cytotoxin associated gene (cagA) were performed. s1/m2 was the most prevalent vacA genotype in both studied groups. There was no association between cagA gene status and disease outcome as nearly all of the isolated strains were cagA positive. According to the serological studies, host responses toward Hp virulence markers (mainly CagA and VacA) were similar in gastric cancer (GC) and non GC patients. Furthermore, host antibody responses to 3.5 kDa and 37kDa antigenes were more frequent in non GC subjects and were inversely associated with GC. This study reveals that cagA gene status or antibody response thereto does not seem to be a suitable marker in screening Hp infected population in risk of gastric cancer development.