How Exactly Does FKBP Work?

Appropriate preoperative cessation of treatment appeared to reduce this risk; however, caution must be taken with regard to the systemic risk associated with cessation of therapy. ""To clarify the effects of a single-nucleotide polymorphism, rs4236601[A] near caveolin SRT1720 1 and 2, on primary open-angle glaucoma (POAG) risk. Meta-analysis. A total of 5774 patients and 40?598 controls from previously reported case�Ccontrol studies were included. A comprehensive literature search was performed for studies published up to April 2013. Summary odds ratios (ORs) and 95% confidence intervals (CI) were calculated, employing random- or fixed-effects models according to between-study heterogeneity. Publication bias of the literature articles was evaluated using funnel plots and Egger's test. OR for the effects of rs4236601[A] on POAG risk. Five eligible studies were included in this meta-analysis. Overall, the association between rs4236601[A] and risk for POAG was statistically significant (OR?=?1.23, 95% CI 1.12�C1.34; P?Pexidartinib chemical structure Asian populations. However, well-designed gene�Cenvironment interaction studies and studies including more ethnic groups are required in further investigations. Glaucoma is the second-leading cause of blindness in the world. According to Quigley and Broman, by the year 2020, the number of people in the world with primary glaucoma is expected to increase to 79.6 million, and 74% of these cases will have open-angle glaucoma.[1] Primary open-angle glaucoma (POAG), the most common form of glaucoma, is a complex, heterogeneous disease with a multifactorial etiology that includes factors such as elevated intraocular pressure (IOP), aging, race, gender, family history, oxidative stress, mitochondrial DNA mutations and specific gene mutations.[2-6] FKBP Genetics plays an important role in the pathogenesis of POAG;[5-7] for example, mutations in several genes, such as those for myocilin (MYOC), optineurin (OPTN) and WD repeat domain 36 (WDR36), are causal or associated with increased risk of developing POAG in multiple populations.[8-10] Recently, via genome-wide association study, the genes TMCO1 and CDKN2B-AS1 have been found to be associated with POAG.[11] Association studies have also identified many variants that may contribute to POAG.