Epidemiologic and genetic/molecular research on @entity726 in Iran started within the past decade. A population-based study on the epidemiology of @entity726 in Yazd, a city in central Iran, revealed that 4.4% of studied individuals were affected with @entity726 : 1.6% with high tension @entity725 ( @entity725 ), 1.6% with normal tension @entity725 , and 0.4% each with @entity2747 ( @entity2747 ) and @entity9998 ( @entity9998 ), and other types of @entity726 . Two notable observations were the relatively high frequency of normal tension @entity726 cases (1.6%) and the large fraction of @entity726 affected individuals (nearly 90%) who were unaware of their condition. The first and most subsequent genetic studies on @entity726 in Iran were focused on primary @entity10064 (PCG) showing that @entity4188 ( @entity4188 ) is the cause of PCG in the majority of Iranian @entity1 , many different @entity4188 mutations are present among Iranian @entity1 but only four mutations constitute the vast majority, and the origins of most mutations in the Iranians are @entity5748 ( @entity5748 ) with the same mutations in other populations. Furthermore, most of the PCG @entity1 are from the northern and northwestern provinces of Iran. A statistically significant male predominance of PCG was observed only among @entity1 without @entity4188 mutations. Clinical investigations on family members of PCG @entity1 revealed that @entity4188 mutations exhibit variable expressivity, but almost complete penetrance. A great number of individuals harboring @entity4188 mutations become affected with juvenile onset @entity725 . Screening of JOAG @entity1 showed that an approximately equal fraction of the @entity1 harbor @entity4188 and ( @entity29714 ) @entity29714 mutations; @entity29714 is a well-known adult onset @entity726 causing gene. Presence of @entity4188 mutations in JOAG @entity1 suggests that in some cases, the two conditions may share a common etiology. Further genetic analysis of Iranian PCG @entity1 led to identification of @entity29713 ( @entity29713 ) as a causative gene for both PCG and several diseases which are often accompanied by @entity11962 , such as @entity36640 3 (WMS3). The findings on @entity29713 have contributed to recognize the importance of the extracellular matrix in pathways leading to @entity726 .

@entity726 in iran and contributions of studies in iran to the understanding of the etiology of XXXX .

@entity1 :: ('9606', 'Species') :: ['patients'] @entity725 :: ('MESH:C562750', 'Disease') :: ['POAG', 'primary open angle glaucoma'] @entity29713 :: ('4053', 'Gene') :: ['LTBP2', 'Latent-transforming growth factor beta-binding protein 2'] @entity9998 :: ('MESH:D017889', 'Disease') :: ['PEXG', 'pseudoexfoliation glaucoma'] @entity4188 :: ('1545', 'Gene') :: ['CYP1B1', 'cytochrome P450 1B1'] @entity5748 :: ('MESH:D009105', 'Disease') :: ['IBD', 'identical by descent'] @entity726 :: ('MESH:D005901', 'Disease') :: ['glaucoma', 'secondary glaucoma'] @entity11962 :: ('MESH:D001946', 'Disease') :: ['glaucomatous presentations'] @entity36640 :: ('MESH:D056846', 'Disease') :: ['Weill-Marchesani syndrome'] @entity10064 :: ('MESH:C565547', 'Disease') :: ['congenital glaucoma'] @entity2747 :: ('MESH:D015812', 'Disease') :: ['PACG', 'primary angle closure glaucoma'] @entity29714 :: ('4653', 'Gene') :: ['MYOC', 'myocilin']
@entity726 :: (MESH:D005901,Disease) :: ['glaucoma']
