Ophthalmology, Eye and Vision Research Collected Works

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    Accurate Imputation-Based Screening of Gln368Ter Myocilin Variant in Primary Open-Angle Glaucoma
    (Association for Research in Vision and Ophthalmology, 2015-08) Gharahkhani, Puya ; Burdon, Kathryn Penelope ; Hewitt, Alex W ; Law, Matthew H ; Souzeau, Emmanuelle ; Montgomery, Grant W ; Radford-Smith, Graham ; Mackey, David A ; Craig, Jamie E ; MacGregor, Stuart
    PURPOSE: Myocilin (MYOC) is a well-established primary open-angle glaucoma (POAG) risk gene, with rare variants known to have high penetrance. The most common clinically relevant risk variant, Gln368Ter, has an allele frequency of 0.1% to 0.3% in populations of European ancestry. Detection of rare MYOC variants has traditionally been conducted using Sanger sequencing. Here we report the use of genotyping arrays and imputation to assess whether rare variants including Gln368Ter can be reliably detected. METHODS: A total of 1155 cases with advanced POAG and 1992 unscreened controls genotyped on common variant arrays participated in this study. Accuracy of imputation of Gln368Ter variants was compared with direct sequencing. A genome-wide association study was performed using additive model adjusted for sex and the first six principal components. RESULTS: We found that although the arrays we used were designed to tag common variants, we could reliably impute the Gln368Ter variant (rs74315329). When tested in 1155 POAG cases and 1992 controls, rs74315329 was strongly associated with risk (odds ratio = 15.53, P = 1.07 × 10-9). All POAG samples underwent full sequencing of the MYOC gene, and we found a sensitivity of 100%, specificity of 99.91%, positive predictive value of 95.65%, and negative predictive value of 100% between imputation and sequencing. Gln368Ter was also accurately imputed in a further set of 1801 individuals without POAG. Among the total set of 3793 (1992 + 1801) individuals without POAG, six were predicted (probability > 95%) to carry the risk variant. CONCLUSIONS: We demonstrate that some clinically important rare variants can be reliably detected using arrays and imputation. These results have important implications for the detection of clinically relevant incidental findings in ongoing and future studies using arrays.
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    Analysis combining correlated glaucoma traits identifies five new risk loci for open-angle glaucoma
    (Nature Publishing Group, 2018-02-18) Gharahkhani, Puya ; Burdon, Kathryn Penelope ; Cooke-Bailey, Jessica N ; Hewitt, Alex W ; Law, Matthew H ; Pasquale, Louis R ; Kang, Jae Hee ; Haines, Jonathan L ; Souzeau, Emmanuelle ; Zhou, Tiger ; Siggs, Owen M ; Landers, John ; Awadalla, Mona S ; Sharma, Shiwani ; Mills, Richard Arthur ; Ridge, Bronwyn ; Lynn, David J ; Casson, Robert J ; Graham, Stuart L ; Goldberg, Ivan ; White, Andrew J ; Healey, Paul R ; Grigg, John RB ; Lawlor, Mitchell ; Mitchell, Paul ; Ruddle, Jonathan B ; Coote, Michael A ; Walland, Mark ; Best, Stephen ; Vincent, Andrea ; Gale, Jesse ; Radford-Smith, Graham ; Whiteman, David C ; Montgomery, Grant W ; Martin, Nicholas G ; Mackey, David A ; Wiggs, Janey L ; MacGregor, Stuart ; Craig, Jamie E ; Neighborhood Consortium
    Open-angle glaucoma (OAG) is a major cause of blindness worldwide. To identify new risk loci for OAG, we performed a genome-wide association study in 3,071 OAG cases and 6,750 unscreened controls, and meta-analysed the results with GWAS data for intraocular pressure (IOP) and optic disc parameters (the overall meta-analysis sample size varying between 32,000 to 48,000 participants), which are glaucoma-related traits. We identified and independently validated four novel genome-wide significant associations within or near MYOF and CYP26A1, LINC02052 and CRYGS, LMX1B, and LMO7 using single variant tests, one additional locus (C9) using gene-based tests, and two genetic pathways - “response to fluid shear stress” and “abnormal retina morphology” - in pathway-based tests. Interestingly, some of the new risk loci contribute to risk of other genetically-correlated eye diseases including myopia and age-related macular degeneration. To our knowledge, this study is the first integrative study to combine genetic data from OAG and its correlated traits to identify new risk variants and genetic pathways, highlighting the future potential of combining genetic data from genetically-correlated eye traits for the purpose of gene discovery and mapping.
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    Angiogenic and Immunologic Proteins Identified by Deep Proteomic Profiling of Human Retinal and Choroidal Vascular Endothelial Cells: Potential Targets for New Biologic Drugs
    (Elsevier, 2018-03-17) Smith, Justine R ; David, Larry L ; Appukuttan, Binoy ; Wilmarth, Phillip A
    Purpose Diseases that involve retinal or choroidal vascular endothelial cells are leading causes of vision loss: age-related macular degeneration, retinal ischemic vasculopathies, and noninfectious posterior uveitis. Proteins differentially expressed by these endothelial cell populations are potential drug targets. We used deep proteomic profiling to define the molecular phenotype of human retinal and choroidal endothelial cells at the protein level. Methods Retinal and choroidal vascular endothelial cells were separately isolated from 5 human eye pairs by selection on CD31. Total protein was extracted and digested, and peptide fractions were analyzed by reverse-phase liquid chromatography tandem mass spectrometry. Peptide sequences were assigned to fragment ion spectra, and proteins were inferred from openly accessible protein databases. Protein abundance was determined by spectral counting. Publicly available software packages were used to identify proteins that were differentially expressed between human retinal and choroidal endothelial cells, and to classify proteins that were highly abundant in each endothelial cell population. Results Human retinal and/or choroidal vascular endothelial cells expressed 5042 nonredundant proteins. Setting the differential expression false discovery rate at 0.05, 498 proteins of 3454 quantifiable proteins (14.4%) with minimum mean spectral counts of 2.5 were differentially abundant in the 2 cell populations. Retinal and choroidal endothelial cells were enriched in angiogenic proteins, and retinal endothelial cells were also enriched in immunologic proteins. Conclusions This work describes the different protein expression profiles of human retinal and choroidal vascular endothelial cells, and provides multiple candidates for further study as novel treatments or drug targets for posterior eye diseases.
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    Angiopoietin receptor TEK mutations underlie primary congenital glaucoma with variable expressivity
    (American Society for Clinical Investigation, 2016) Souma, Tomokazu ; Tompson, Stuart W ; Thomson, Benjamin R ; Siggs, Owen M ; Kizhatil, Krishnakumar ; Yamaguchi, Shinji ; Feng, Liang ; Limviphuvadh, Vachiranee ; Whisenhunt, Kristina N ; Maurer-Stroh, Sebastian ; Yanovitch, Tammy L ; Kalaydijieva, Luba ; Azmanov, Dimitar N ; Finzi, Simone ; Mauri, Lucia ; Javadiyan, Shahrbanou ; Souzeau, Emmanuelle ; Zhou, Tiger ; Hewitt, Alex W ; Kloss, Bethany ; Burdon, Kathryn Penelope ; Mackey, David A ; Allen, Keri F ; Ruddle, Jonathan B ; Lim, Sing-Hui ; Rozen, Steve ; Tran-Viet, Khanh-Nhat ; Liu, Xiaorong ; John, Simon ; Wiggs, Janey L ; Pasutto, Francesca ; Craig, Jamie E ; Jin, Jing ; Quaggin, Susan ; Young, Terri L
    Primary congenital glaucoma (PCG) is a devastating eye disease and an important cause of childhood blindness worldwide. In PCG, defects in the anterior chamber aqueous humor outflow structures of the eye result in elevated intraocular pressure (IOP); however, the genes and molecular mechanisms involved in the etiology of these defects have not been fully characterized. Previously, we observed PCG-like phenotypes in transgenic mice that lack functional angiopoietin-TEK signaling. Herein, we identified rare TEK variants in 10 of 189 unrelated PCG families and demonstrated that each mutation results in haploinsufficiency due to protein loss of function. Multiple cellular mechanisms were responsible for the loss of protein function resulting from individual TEK variants, including an absence of normal protein production, protein aggregate formation, enhanced proteasomal degradation, altered subcellular localization, and reduced responsiveness to ligand stimulation. Further, in mice, hemizygosity for Tek led to the formation of severely hypomorphic Schlemm’s canal and trabecular meshwork, as well as elevated IOP, demonstrating that anterior chamber vascular development is sensitive to Tek gene dosage and the resulting decrease in angiopoietin-TEK signaling. Collectively, these results identify TEK mutations in patients with PCG that likely underlie disease and are transmitted in an autosomal dominant pattern with variable expressivity.
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    Angiopoietin-1 is required for Schlemm’s canal development in mice and humans
    (American Society for Clinical Investigation, 2017-11) Thomson, Benjamin R ; Souma, Tomokazu ; Tompson, Stuart W ; Onay, Tuncer ; Kizhatil, Krishnakumar ; Siggs, Owen M ; Feng, Liang ; Whisenhunt, Kristina N ; Yanovitch, Tammy L ; Kalaydjieva, Luba ; Azmanov, Dimitar N ; Finzi, Simone ; Tanna, Christine A ; Hewitt, Alex W ; Mackey, David A ; Bradfield, Yasmin S ; Souzeau, Emmanuelle ; Javadiyan, Shahrbanou ; Wiggs, Janey L ; Pasutto, Francesca ; Liu, Xiaorong ; John, Simon W M ; Craig, Jamie E ; Jin, Jing ; Young, Terri L ; Quaggin, Susan
    Primary congenital glaucoma (PCG) is a leading cause of blindness in children worldwide and is caused by developmental defects in 2 aqueous humor outflow structures, Schlemm’s canal (SC) and the trabecular meshwork. We previously identified loss-of-function mutations in the angiopoietin (ANGPT) receptor TEK in families with PCG and showed that ANGPT/TEK signaling is essential for SC development. Here, we describe roles for the major ANGPT ligands in the development of the aqueous outflow pathway. We determined that ANGPT1 is essential for SC development, and that Angpt1-knockout mice form a severely hypomorphic canal with elevated intraocular pressure. By contrast, ANGPT2 was dispensable, although mice deficient in both Angpt1 and Angpt2 completely lacked SC, indicating that ANGPT2 compensates for the loss of ANGPT1. In addition, we identified 3 human subjects with rare ANGPT1 variants within an international cohort of 284 PCG patients. Loss of function in 2 of the 3 patient alleles was observed by functional analysis of ANGPT1 variants in a combined in silico, in vitro, and in vivo approach, supporting a causative role for ANGPT1 in disease. By linking ANGPT1 with PCG, these results highlight the importance of ANGPT/TEK signaling in glaucoma pathogenesis and identify a candidate target for therapeutic development.
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    An Anti–VEGF-B Antibody Fragment Induces Regression of Pre-Existing Blood Vessels in the Rat Cornea
    (ARVO Journals, 2017-07) Irani, Yazad ; Scotney, Pierre ; Klebe, Sonja ; Mortimer, Lauren A ; Nash, Andrew ; Williams, Keryn Anne
    Purpose: We tested the ability of an antibody fragment with specificity for vascular endothelial growth factor-B (VEGF-B) to regress nascent and established corneal blood vessels in the rat. Methods: A single chain variable antibody fragment (scFv) with specificity for VEGF-B was engineered from the 2H10 hybridoma. Binding to rat, mouse, and human VEGF-B was confirmed by surface plasmon resonance. Activity of the anti–VEGF-B scFv on developing and established corneal blood vessels was assessed following unilateral superficial cautery in male and female outbred Sprague Dawley rats. Groups (untreated, control scFv-treated, or anti–VEGF-B scFv-treated) comprised 6 to 22 rats. Treatment consisted of 5 μL scFv, 1 mg/mL, applied topically five times per day for 14 days, or two subconjunctival injections, 50 μg scFv each, applied 7 days apart, or combined topical and subconjunctival treatment. Corneal vessel area was quantified on hematoxylin-stained corneal flat-mounts, and groups were compared using the Mann-Whitney U test, with post hoc Bonferroni correction. Immunohistochemistry for cleaved caspase-3 was performed. Results: Topical anti–VEGF-B scFv therapy alone did not regress corneal blood vessels significantly (P > 0.05). Subconjunctival injection and combined treatment regressed 14-day established corneal blood vessels (25% reduction in vessel area [P = 0.04] and 37% reduction in vessel area [P < 0.001], respectively, compared to results in untreated controls). Cleaved caspase-3 was identified in vascular endothelial cells of anti–VEGF-B scFv-treated corneas. In scFv-treated rats, corneal endothelial cell function was maintained to 12 weeks after treatment and a normal blink reflex was present. Conclusions: The anti–VEGF-B scFv significantly regressed established but not developing corneal blood vessels in rats.
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    Assessment of Cataract Surgery Outcome Using the Modified Catquest Short-Form Instrument in China
    (PLOS, 2016-10-13) Khadka, Jyoti ; Huang, Jinhai ; Chen, Haisi ; Chen, Chengwei ; Gao, Rongrong ; Bao, Fangjun ; Zhang, Sifang ; Wang, Qinmei ; Pesudovs, Konrad
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    Assessment of corneal thickness measurement using swept-source Fourier-domain anterior segment optical coherence tomography and Scheimpflug camera
    (Elsevier, 2012-07-01) Huang, Jinhai ; Feng, Yifan ; Wang, Qinmei ; Pesudovs, Konrad
    No abstract available
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    Assessment of polygenic effects links primary open-angle glaucoma and age-related macular degeneration
    (Nature Publishing Group, 2016) Cuellar-Partida, Gabriel ; Craig, Jamie E ; Burdon, Kathryn Penelope ; Wang, Jie Jin ; Vote, Brendan J ; Souzeau, Emmanuelle ; McAllister, Ian L ; Isaacs, Timothy ; Lake, Stewart ; Mackey, David A ; Constable, Ian J ; Mitchell, Paul ; Hewitt, Alex W ; MacGregor, Stuart
    Primary open-angle glaucoma (POAG) and age-related macular degeneration (AMD) are leading causes of irreversible blindness. Several loci have been mapped using genome-wide association studies. Until very recently, there was no recognized overlap in the genetic contribution to AMD and POAG. At genome-wide significance level, only ABCA1 harbors associations to both diseases. Here, we investigated the genetic architecture of POAG and AMD using genome-wide array data. We estimated the heritability for POAG (h2 g = 0.42 ± 0.09) and AMD (h2 g = 0.71 ± 0.08). Removing known loci for POAG and AMD decreased the h2 g estimates to 0.36 and 0.24, respectively. There was evidence for a positive genetic correlation between POAG and AMD (rg = 0.47 ± 0.25) which remained after removing known loci (rg = 0.64 ± 0.31). We also found that the genetic correlation between sexes for POAG was likely to be less than 1 (rg = 0.33 ± 0.24), suggesting that differences of prevalence among genders may be partly due to heritable factors.
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    Association of eNOS polymorphisms with primary angle-closure glaucoma
    (Association for Research in Vision and Ophthalmology, 2013-03) Awadalla, Mona S ; Thapa, Suman S ; Hewitt, Alex W ; Craig, Jamie E ; Burdon, Kathryn Penelope
    Purpose: Recently, several studies have investigated genetic associations between Cytochrome P450 (CYP1B1), Endothelial nitric oxide synthase (eNOS) and Neurotrophin-4 (NTF4) with primary angle-closure glaucoma (PACG) in various ethnic groups. Here we investigate the association of these candidate genes with PACG in samples from Australia and Nepal. Method: A total of 235 patients with PACG (106 Nepalese and 129 Australian) and 492 controls (204 Nepalese and 288 Australian) were included. Tag single nucleotide polymorphisms (SNPs) were selected to cover the majority of common variation within the candidate genes and genotyped in DNA extracted from peripheral whole blood. Allele and haplotype analyses were conducted in PLINK. Bonferroni correction was applied for the total number of SNPs in this study (p=0.05/15=0.003) Results: In the Australian cohort, one eNOS SNP rs3793342 shows significance association with PACG in the Australian cohort after Bonferroni correction (p-value 0.003, OR 0.5 95% CI 0.3-0.8). After adjusting the results for sex and age both SNPs rs3793342 and rs7830 showed significance after Bonferroni correction (p-value of 0.001 and 0.003, respectively). The eNOS haplotype of all 7 typed SNPs showed significant association with a global p-value of 0.019, with the CGCAATC haplotype giving a specific p-value of 0.008 and odds ratio of 1.5 (95% CI 0.9-2.4). In the Nepalese cohort, SNPs in CYP1B1 and NTF4 genes showed borderline association with PACG but did not survive Bonferroni correction. Conclusions: The present data support the involvement of common variations in eNOS with PACG pathogenesis. Differences were observed in the two populations studied, and additional replication studies in other populations are necessary to confirm these associations
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    Association of genetic variants in the TMCO1 gene with clinical parameters related to glaucoma and characterisation of the protein in the eye
    (Association for Research in Vision and Ophthalmology, 2012-06-06) Sharma, Shiwani ; Burdon, Kathryn Penelope ; Chidlow, Glyn ; Klebe, Sonja ; Crawford, April ; Dimasi, David Paul ; Dave, Alpana ; Martin, Sarah ; Javadiyan, Shahrbanou ; Wood, John P M ; Casson, Robert J ; Danoy, Patrick ; Griggs, Kim Marie ; Hewitt, Alex W ; Landers, John ; Mitchell, Paul ; Mackey, David A ; Craig, Jamie E
    Purpose. Glaucoma is the leading cause of irreversible blindness worldwide. Primary open angle glaucoma (POAG) is the most common subtype. We recently reported association of genetic variants at chromosomal loci, 1q24 and 9p21, with POAG. In this study, we determined association of the most significantly associated single nucleotide polymorphism (SNP) rs4656461, at 1q24 near the TMCO1 gene, with the clinical parameters related to glaucoma risk and diagnosis, and determined ocular expression and subcellular localization of the human TMCO1 protein to understand the mechanism of its involvement in POAG. Methods. Association of SNP rs4656461 with five clinical parameters was assessed in 1420 POAG cases using linear regression. The TMCO1 gene was screened for mutations in 95 cases with a strong family history and advanced disease. Ocular expression and subcellular localization of the TMCO1 protein were determined by immunolabeling and as GFP-fusion. Results. The data suggest that individuals homozygous for the rs4656461 risk allele (GG) are 4 to 5 years younger at diagnosis than noncarriers of this allele. Our data demonstrate expression of the TMCO1 protein in most tissues in the human eye, including the trabecular meshwork and retina. However, the subcellular localization differs from that reported in other studies. We demonstrate that the endogenous protein localizes to the cytoplasm and nucleus in vivo and ex vivo. In the nucleus, the protein localizes to the nucleoli. Conclusions. This study shows a relationship between genetic variation in and around TMCO1 with age at diagnosis of POAG and provides clues to the potential cellular function/s of this gene.
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    Association of genetic variants with primary angle closure glaucoma in two different populations
    (Public Library of Science, 2013) Awadalla, Mona S ; Thapa, Suman S ; Hewitt, Alex W ; Burdon, Kathryn Penelope ; Craig, Jamie E
    PURPOSE: A recent large genome-wide association study (GWAS) identified multiple variants associated with primary angle-closure glaucoma (PACG). The present study investigated the role of these variants in two cohorts with PACG recruited from Australia and Nepal. METHOD: Patients with PACG and appropriate controls were recruited from eye clinics in Australia (n = 232 cases and n = 288 controls) and Nepal (n = 106 cases and 204 controls). Single nucleotide polymorphisms (SNPs) rs3753841 (COL11A1), rs1015213 (located between PCMTD1 and ST18), rs11024102 (PLEKHA7), and rs3788317 (TXNRD2) were selected and genotyped on the Sequenom. Analyses were conducted using PLINK and METAL. RESULTS: After adjustment for age and sex, SNP rs3753841 was found to be significantly associated with PACG in the Australian cohort (p = 0.017; OR = 1.34). SNPs rs1015213 (p = 0.014; OR 2.35) and rs11024102 (p = 0.039; OR 1.43) were significantly associated with the disease development in the Nepalese cohort. None of these SNPs survived Bonferroni correction (p = 0.05/4 = 0.013). However, in the combined analysis, of both cohorts, rs3753841 and rs1015213 showed significant association with p-values of 0.009 and 0.004, respectively both surviving Bonferroni correction. SNP rs11024102 showed suggestive association with PACG (p-value 0.035) and no association was found with rs3788317. CONCLUSION: The present results support the initial GWAS findings, and confirm the SNP's contribution to PACG. This is the first study to investigate these loci in both Australian Caucasian and Nepalese populations.
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    Association of open-angle glaucoma loci with incident glaucoma in the Blue Mountains Eye Study.
    (Elsevier Inc., 2015) Burdon, Kathryn Penelope ; Mitchell, Paul ; Lee, Anne ; Healey, Paul R ; White, Andrew J ; Rochtchina, Elena ; Thomas, P ; Wang, Jie Jin ; Craig, Jamie E
    PURPOSE: To determine if open-angle glaucoma (OAG)-associated single nucleotide polymorphisms (SNPs) are associated with incident glaucoma and if such genetic information is useful in OAG risk prediction. DESIGN: Case-control from within a population-based longitudinal study. METHODS: study population: Individuals aged over 49 years of age living in the Blue Mountains region west of Sydney and enrolled in the Blue Mountains Eye Study. observation: Cases for this sub-study (n = 67) developed incident OAG between baseline and 10-year visits, in either eye, while controls (n = 1919) had no evidence for OAG at any visit. All participants had an ocular examination and DNA genotyped for reported OAG risk SNPs. main outcome measure: Incident OAG. RESULTS: Two loci also known to be associated with cup-to-disc ratio as well as OAG (9p21 near CDKN2B-AS1 and SIX1/SIX6) were both significantly associated with incident OAG in the Blue Mountains Eye Study cohort (P = .006 and P = .004, respectively). The TMCO1 locus was nominally associated (P = .012), while the CAV1/CAV2 and 8q22 loci were not associated. Multivariate logistic regression and neural network analysis both indicated that the genetic risk factors contributed positively to the predictive models incorporating traditional risk factors. CONCLUSIONS: This study shows that previously reported genetic variations related to OAG and cup-to-disc ratio are associated with the onset of OAG and thus may become useful in risk prediction algorithms designed to target early treatment to those most at risk of developing glaucoma.
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    Australian and New Zealand Registry of Advanced Glaucoma: methodology and recruitment
    (Wiley-Blackwell, 2013-08-13) Souzeau, Emmanuelle ; Goldberg, Ivan ; Healey, Paul R ; Mills, Richard Arthur ; Landers, John ; Graham, Stuart L ; Grigg, John RB ; Usher, Bronwyn ; Straga, Tania ; Crawford, April ; Casson, Robert J ; Morgan, William H ; Ruddle, Jonathan B ; Coote, Michael A ; White, Andrew J ; Stewart, James ; Hewitt, Alex W ; Mackey, David A ; Burdon, Kathryn Penelope ; Craig, Jamie E
    Glaucoma is a sight-threatening disease affecting 3% of the population over the age of 50. Glaucoma is treatable, and severe vision loss can usually be prevented if diagnosis is made at an early stage. Genetic factors play a major role in the pathogenesis of the condition, and therefore, genetic testing to identify asymptomatic at-risk individuals is a promising strategy to reduce the prevalence of glaucoma blindness. Furthermore, unravelling genetic risk factors for glaucoma would also allow a better understanding of the pathogenesis of the condition and the development of new treatments. With the collection of glaucoma cases recruited so far, our registry aims to identify novel glaucoma genetic risk factors to establish risk profiling of the population and protocols for genetic testing.
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    The Australian Corneal Graft Registry 2004 annual report
    ( 2006-06-20T03:38:28Z) Williams, Keryn Anne ; Hornsby, Ngaere B ; Bartlett, Christine Mary ; Holland, Helene K ; Esterman, Adrian Jeffrey ; Coster, Douglas John
    The Australian Corneal Graft Registry (ACGR) opened in May 1985 and has now been in operation for 18 years. In that time, we have collected data on over 14,000 corneal grafts. At the time of transplantation, we seek information on the recipient, the donor and the operative procedure. Follow-up then occurs at approximately yearly intervals for an indefinite period. Follow-up only ceases upon loss of the graft, or death or loss-to-follow-up of the patient. At each round of follow-up, we request information on graft and visual outcome, and upon relevant events and treatments. The data are entered into a database and checked for consistency. Descriptive, univariate and multivariate analyses are performed, and the report collated.
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    The Australian Corneal Graft Registry 2007 Report
    (Flinders University Press, 2007) Williams, Keryn Anne ; Lowe, Marie Therese ; Bartlett, Christine Mary ; Kelly, L ; Coster, Douglas John
    The Australian Corneal Graft Registry opened in May 1985 and thus has now been in operation for over 22 years. The census date for this report was 01/09/2006. Over the years, we have collected data on more than 18,500 corneal grafts. The majority of corneal grafts registered have been penetrating, but increasing numbers of lamellar and limbal grafts have also been registered over recent years, as patterns of surgical practice change. At registration, we seek information on the recipient, the donor, the eye bank practices and the operative procedure. Follow-up then occurs at approximately yearly intervals for an indefinite period, and ceases upon loss of the graft, or the death or loss-to-follow-up of the patient. At each round of follow-up, we request information on the graft and visual outcome, and upon relevant post-operative events and treatments. The data are entered into an Access database and checked for consistency. Descriptive, univariate and multivariate analyses are subsequently performed using SPSS and Stata software, and the report is eventually collated.
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    The Australian Corneal Graft Registry 2012 Report
    ( 2012-03-09) Williams, Keryn Anne ; Lowe, Marie Therese ; Keane, Miriam Claire ; Jones, Victoria J ; Loh, Raymond S K ; Coster, Douglas John
    The Australian Corneal Graft Registry (ACGR) opened in May 1985 and thus has now been in operation for over 26 years. However, the census dates for this report was 01/06/2010 for penetrating grafts and 12/10/2011 for lamellar grafts. Over the years, we have collected data on more than 23,000 corneal grafts. The majority of corneal grafts registered have been penetrating, but increasing numbers of lamellar grafts have also been registered over recent years, as patterns of surgical practice change. At registration, we seek information on the recipient, the donor, the eye bank practices and the operative procedure. Follow-up then occurs at approximately yearly intervals for an indefinite period, and ceases upon loss of the graft, or the death or loss-to-follow-up of the patient. At each round of follow-up, we request information on the graft and visual outcome, and upon relevant post-operative events and treatments. The data are entered into an Access database and checked for consistency. Descriptive, univariate and multivariate analyses are subsequently performed using SPSS and Stata software, and the report is eventually collated.
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    The Australian Corneal Graft Registry 2012 Report
    ( 2012-03-05) Williams, Keryn Anne ; Lowe, Marie Therese ; Keane, Miriam Claire ; Jones, Victoria J ; Loh, Raymond S K ; Coster, Douglas John
    The Australian Corneal Graft Registry (ACGR) opened in May 1985 and thus has now been in operation for over 26 years. However, the census dates for this report was 01/06/2010 for penetrating grafts and 12/10/2011 for lamellar grafts. Over the years, we have collected data on more than 23,000 corneal grafts. The majority of corneal grafts registered have been penetrating, but increasing numbers of lamellar grafts have also been registered over recent years, as patterns of surgical practice change. At registration, we seek information on the recipient, the donor, the eye bank practices and the operative procedure. Follow-up then occurs at approximately yearly intervals for an indefinite period, and ceases upon loss of the graft, or the death or loss-to-follow-up of the patient. At each round of follow-up, we request information on the graft and visual outcome, and upon relevant post-operative events and treatments. The data are entered into an Access database and checked for consistency. Descriptive, univariate and multivariate analyses are subsequently performed using SPSS and Stata software, and the report is eventually collated.
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    The Australian Corneal Graft Registry 2015 Report
    (South Australian Health and Medical Research Institute, 2015-06-15) Williams, Keryn Anne ; Keane, Miriam Claire ; Galettis, Rachel A ; Jones, Victoria J ; Mills, Richard Arthur ; Coster, Douglas John
    The Australian Corneal Graft Registry (ACGR) opened in May 1985 and has now been operating for 30 years. Over the years, we have collected information on more than 30,000 corneal grafts. At registration, we seek information on the donor, eye bank practices, the recipient, the surgeon, the graft type and the operative procedure. Follow-up then occurs at approximately yearly intervals for an indefinite period, and ceases upon graft failure, or the death or loss-to-follow-up of the patient. At each round of follow-up, we request information on the survival of the graft, the visual outcomes, and any relevant post-operative events and treatments. The data are entered into an Access database and checked for consistency. Descriptive, univariate and multivariate analyses are subsequently performed using SPSS and Stata software, and the report is eventually collated.
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    The Australian Corneal Graft Registry 2018 Report
    (South Australian Health and Medical Research Institute, 2018) Williams, Keryn Anne ; Keane, Miriam Claire ; Coffey, Nora Elizabeth ; Jones, Victoria Jane ; Mills, Richard Arthur ; Coster, Douglas John
    The Australian Corneal Graft Registry (ACGR) opened in May 1985 and has now been operating for 33 years. Over the years, we have collected information on more than 35,000 corneal grafts. At registration, we seek information on the donor, eye bank practices, the recipient, the surgeon, the graft type and the operative procedure. Follow-up then occurs at approximately yearly intervals for an indefinite period, and ceases upon graft failure, or the death or loss-to-follow-up of the patient. At each round of follow-up, we request information on the survival of the graft, the visual outcomes, and any relevant post-operative events and treatments. The data are entered into an Access database and checked for consistency. Descriptive, univariate and multivariate analyses are subsequently performed using SPSS and Stata software, and the report is eventually collated.