’’’’..اختلافات جينيه مسببه للصدفيه..’’’’

[جودينا]

بســــم الله الرحمن الرحيــــم

Gene variation is 'major genetic determinant of psoriasis'

People with 3 independent genetic variants are 9 times more likely to get disease

(SALT LAKE CITY)—A specific genetic region that has been increasingly identified as the strongest genetic link to psoriasis has an even more significant role in the chronic skin disease than has been suspected, University of Utah medical researchers show in a new study.
In the Aug. 13 issue of PLoS Genetics, researchers in the U School of Medicine's Department of Dermatology confirm that the presence of HLA-Cw*0602, a gene variation or allele on chromosome 6 found to be associated with psoriasis by numerous investigators, is the "major genetic determinant" of psoriasis, but that other nearby genetic variations also play an independent role in contributing to the disease
"The HLA-Cw*0602 gene variation stands alone as a high risk for psoriasis," said Gerald G. Krueger, M.D., professor of dermatology, Benning Presidential Endowed Chair holder, and a co-author on the study. "A major question has been: are there other genetic variations in this region that associate with psoriasis?"
The study reported in PLoS Genetics identifies two other genetic variations on chromosome 6 that also have significant association with psoriasis. People who have all three genetic variations are nearly nine times more at risk for psoriasis.
Psoriasis is a chronic disease that causes red scaly patches on the skin and affects up to 7.5 million people in the United States. About 25 percent of subjects with the disease also develop a painful inflammation of the joints called psoriatic arthritis.
University researchers, led by first author Bing-Jian Feng, Ph.D., postdoctoral fellow, and senior author David E. Goldgar, Ph.D., research professor of dermatology in the U of U School of Medicine, reached their conclusion after an expanded analysis of data from a study published earlier this year by investigators at Utah in collaboration with colleagues from the University of Michigan and Washington University.
That study (Nature Genetics, Jan. 25) used new technology to scan nearly 500,000 genetic variants (single nucleotide polymorphisms or SNPs) in 1,359 people with psoriasis and 1,400 without to find those with the strongest relationship with psoriasis. After identifying 18 SNPs with the highest associations with psoriasis, the researchers expanded the study to include 5,048 people with psoriasis and 5,051 without the disease. From that, they identified four new genetic "hotspots" for psoriasis and confirmed two others that Krueger and colleagues identified in previous studies.
Using the data from the Nature Genetics study, Feng, Goldgar, and colleagues employed two statistical methods, imputation and logistic regression analysis, to determine with a much greater degree of accuracy those genes that have the highest association with psoriasis. Using imputation they were able to reliably predict the *0602 status of all subjects in the recent Nature Genetics study. This did two things; first, it increased the confidence that *0602 is the major genetic variation on this chromosome and, second, it permitted them to determine if there was any other associated genetic variation in this region.
Removing the strong effect of *0602 resulted in the identification of two other loci (fixed position on a chromosome) that are independently associated with psoriasis (MICA/HLA-B and c6orf10). These two loci increased the risk for the disease by 1.23 and 1.6 times, respectively. However, when all three genetic variations that Feng, Goldgar, and colleagues report are present, the risk for psoriasis is 8.9 times higher than when none of these is present.
To confirm the results, the researchers examined an independent patient population in China, which corroborated their conclusions.
While *0602 and the associated, but independent, genetic variations reported have a major genetic contribution to psoriasis, many other genes undoubtedly play a role, according to Krueger. The number of DNA sites discovered to have strong associations with psoriasis has more than doubled in the past
two years.

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http://www.eurekalert.org/pub_releas...-gvi082709.php

[جودينا]

اجمالا وبترجمه متواضعه...بعد الدراسات وجدو منطقه اختلال جيني لها الدور الأكبر في ظهور داء الصدفيه

خبر خير ... عرفو سببها ,,,اذن باقي حل او علاج لهذا الاختلال

لنـا عوده

[قاهر الصدفيه]

خبر جيد
انشاء الله يعرفون السبب
(اذا عرف السبب بطل العجب)
تحياتي جودينا

[جودينا]

تشير الدراسات المسْحية إلى أن مرض الصدفية يصيب الجنسين بالتساوي، ويمكن أن تقع الإصابة به في أية سن، وإن كان غالباً ما يظهر بين سني 15 و25 عاماً. ويبلغ انتشار الصدفية بين المجتمعات الغربية والأوروبية نسبة 3% من السكان، ثلثهم مصابون بالدرجة المتوسطة أو الشديدة من المرض. وفي نسبة كبيرة من المرضى، يمكن الاستدلال على تاريخ إصابة أحد أفراد العائلة بالمرض، وهو ما يرجح وجود عامل وراثي، يلعب دوراً مهماً في احتمالات الإصابة. وهذه العلاقة دفعت بالعديد من العلماء إلى بذل جهود مكثفة في محاولة التعرف على الجينات المعيبة لدى الأشخاص التي تؤدي إلى إصابتهم بالصدفية. ففي العدد الأخير من إحدى الدوريات المعنية بعلوم الوراثة (Nature Genetics)، أجرى فريق مكون من علماء من الولايات المتحدة والصين وإسبانيا دراسة مطولة على الآلاف من مرضى الصدفية، تمكنوا خلالها من تحديد نقاط الخلل الجينية، وهو ما يبشر بتطوير علاج أكثر فعالية للمرض في المستقبل، يعتمد على إصلاح الخلل الوراثي الذي يجعل البعض يصابون بالصدفية.


الله يشفينا ومرضى المسلمين

[أبو كامل]

آآآآآآآآآمين
ربي يوفقهم للعلاج

يعطيك العافية جودينا

أبو كامل
المدينة المنورة

[reem50]

شكرا جودينا وبارك الله بك امل جديد في ايجاد علاج نهائي للصدفيه
والله هذا القسم رائع الكل يعمل ويبحث بجد ومثابره للوصول الى هدف واحد
وعندي امل كبير ان نكون على الاقل اول الناس اللي يستفادون من اي علاج جديد لان في القسم هذا متابعين لاخبار الصدفيه اول باول
الله يمن عليكم جميعا بالشفاء العاجل

[ايهاب العراقي]

مشكورة جودينا خوش معلومات...ان شاء الله خير

[ألانوار]

شكرا جودينا

[بنت العم]

مشكوووورة جودينا
معلومات جدا مفيدة

[أم فرفورة]

شكرا ياجودينا تحت اي سبب يارب اشفينا وهدي بالنا يارب