İzmir‐Ankara suture as a Triassic to Cretaceous plate boundary – data from central Anatolia

The İzmir‐Ankara suture represents part of the boundary between Laurasia and Gondwana along which a wide Tethyan ocean was subducted. In northwest Turkey, it is associated with distinct oceanic subduction‐accretion complexes of Late Triassic, Jurassic and Late Cretaceous ages. The Late Triassic and Jurassic accretion complexes consist predominantly of basalt with lesser amounts of shale, limestone, chert, Permian (274 Ma zircon U‐Pb age) metagabbro and serpentinite, which have undergone greenschist facies metamorphism. Ar‐Ar muscovite ages from the phyllites range from 210 Ma down to 145 Ma with a broad southward younging. The Late Cretaceous subduction‐accretion complex, the ophiolitic mélange, consists of basalt, radiolarian chert, shale and minor amounts of recrystallized limestone, serpentinite and greywacke, showing various degrees of blueschist facies metamorphism and penetrative deformation. Ar‐Ar phengite ages from two blueschist metabasites are ca. 80 Ma (Campanian). The ophiolitic mélange includes large Jurassic peridotite‐gabbro bodies with plagiogranites with ca. 180 Ma U‐Pb zircon ages. Geochronological and geological data show that Permian to Cretaceous oceanic lithosphere was subducted north under the Pontides from the Late Triassic to the Late Cretaceous. This period was characterized generally by subduction‐accretion, except in the Early Cretaceous, when subduction‐erosion took place. In the Sakarya segment all the subduction accretion complexes, as well as the adjacent continental sequences, are unconformably overlain by Lower Eocene red beds. This, along with the stratigraphy of the Sakarya Zone indicate that the hard collision between the Sakarya Zone and the Anatolide‐Tauride Block took place in Paleocene

?F508, ?I507 ve F508C kistik fibroz mutasyonlarının gerçek-zamanlı multipleks PCR ile hızlı analizleri

Purpose: Cystic fibrosis, usually seen in childhood, is a hereditary disease that proceeds with the dysfunction of all exocrine glands. The disease is widely spread in Europe, affects the life quality of the affected individuals and causes their early death because of complications resulting from repeatedly serious respiratory tract infections. The most common mutation in cystic fibrosis is ;amp;#916;F508. But so far, more than a thousand of other mutations have been discovered in the cystic fibrosis gene (CFTR); like ;amp;#916;I507 and F508C. F508C and ;amp;#916;F508 mutations are also implicated in the development of congenital vas deferens aplasia. The aim of this study was the rapid analyses of these three mutations that reside in the same CFTR gene region with a real-time multiplex PCR method. Methods: A total of 116 DNA samples of cases coming from the Aegean Region with cystic fibrosis or unilateral vas deferens aplasia were analyzed by a specifically designed real-time multiplex PCR method that detects all three CFTR mutations in one-step. The applied method was also compared with gel electrophoresis and dHPLC methods. Results: Although, we could not detect any carrier for the ;amp;#916;I507 and F508C mutations at the end of our study; 6.0 % of the cases were heterozygous carriers for the ;amp;#916;F508 allele and 1.8 % homozygous ill. The frequency of the ;amp;#916;F508 mutation was defined as 4.7 %. The applied PCR method was also found to be faster in obtaining results compared to gel electrophoresis and dHPLC. Conclusion: The employed real-time multiplex PCR method should be the preferential method for the rapid analysis of the CFTR ;amp;#916;F508, ;amp;#916;I507 and F508C gene mutations in cases with cystic fibrosis or congenital unilateral vas deferens aplasia.Amaç: Kistik fibroz genellikle çocukluk yaşlarında ortaya çıkan ve tüm ekzokrin bezlerin fonksiyon bozukluğu ile seyreden kalıtsal bir hastalıktır. Avrupa' da yaygın olarak görülen bu hastalık kişilerin yaşam kalitesini etkilemekte ve tekrarlayan ağır solunum yolu enfeksiyonlarının açtıkları komplikasyonlar nedeniyle, erken yaşta ölüme yol açmaktadır. Kistik fibroz' daki en yaygın mutasyon ?F508' dir. Bununla birlikte, binden fazla kistik fibroz gen (CFTR) mutasyonu tanımlanmıştır; ?I507 ve F508C gibi. F508C ve ?F508 mutasyonları ayrıca konjenital vas deferens agenezin gelişiminde de rol oynarlar. Çalışmadaki amacımız, aynı CFTR gen bölgesine düşen bu üç mutasyonu gerçek-zamanlı multipleks PCR yöntemi ile hızlı analizlerini gerçekleştirmekti. Gereç ve Yöntem: Ege Bölgesinde yaşayan kistik fibrozlu veya konjenital unilateral vas deferens agenezisi bulunan toplam 116 olgunun DNA örnekleri, tek bir çalışmada üç CFTR mutasyonun ayırıcı tanılarına gidilecek şekilde tasarlanmış olan gerçek zamanlı bir multipleks PCR yöntemiyle çalışıldı. Kullanılan yöntem ayrıca jel elekroforezi ve dHPLC yöntemleriyle de karşılaştırıldı. Bulgular: Çalışmanın sonunda, ?I507 ve F508C mutasyonları için taşıyıcı olgu saptanmamasına karşılık, olguların % 6.0' sı ?F508 aleli için heterozigot taşıyıcı ve % 1.8' i de homozigot hasta bulundu. ?F508 mutasyonunun görülme sıklığı % 4.7 olarak belirlendi. Gerçek-zamanlı multipleks PCR yönteminin jel elektroforezi ve dHPLC' den daha hızlı sonuç verdiği görüldü. Sonuç: Kistik fibrozlu veya konjenital unilateral agenezisi bulunan olgularda CFTR ?F508, ?I507 ve F508C gen mutasyonlarının hızlı tayininde gerçek-zamanlı multipleks PCR ilk tercih edilen yöntem olmalıdır