Ophthalmic Research Journal Impact Factor & Information

Publisher: Karger

Journal description

ëOphthalmic Researchí features original papers, reviews and short communications reporting basic and clinical experimental studies. Authors from throughout the world cover morphologic, physical, physiologic, pharmacological, biochemical and molecular biological aspects of ophthalmology and experimental eye research. Articles on methodological problems are included as well. The results of new experimental research are also interpreted in light of their importance to the clinical work of the eye specialist. This journal provides a record of international research for both researchers and clinicians in ophthalmology.

Current impact factor: 1.38

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 1.376
2012 Impact Factor 1.562
2011 Impact Factor 1.561
2010 Impact Factor 0.847
2009 Impact Factor 1.288
2008 Impact Factor 1.317
2007 Impact Factor 1.25
2006 Impact Factor 1.01
2005 Impact Factor 0.874
2004 Impact Factor 1
2003 Impact Factor 0.975
2002 Impact Factor 0.933
2001 Impact Factor 0.934
2000 Impact Factor 0.773
1999 Impact Factor 1.257
1998 Impact Factor 0.799
1997 Impact Factor 0.627

Impact factor over time

Impact factor
Year

Additional details

5-year impact 1.07
Cited half-life 0.00
Immediacy index 0.22
Eigenfactor 0.00
Article influence 0.33
Website Ophthalmic Research website
Other titles Ophthalmic research
ISSN 0030-3747
OCLC 1761331
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

Karger

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • On author's server or institutional server
    • Server must be non-commercial
    • Publisher's version/PDF cannot be used
    • Publisher copyright and source must be acknowledged
    • Must link to publisher version
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Micro-RNAs (miRNAs) are members of the family of noncoding RNA molecules that regulate gene expression by translational repression and mRNA degradation. Initial identification of miRNAs revealed them only as developmental regulators; later, their radiated roles in various cellular processes have been established. They regulate several pathways, including developmental timing, hematopoiesis, organogenesis, apoptosis, cell differentiation and proliferation. Their roles in eye disorders are being explored by biologists around the world. Eye physiology requires the perfect orchestration of all the regulatory networks; any defect in any of the networks leads to eye disorders. The dysregulation of miRNA expression has been reported in many eye disorders, which paves the way for new therapeutics. This review summarizes the biogenesis of miRNAs and their role in eye disorders. miRNA studies also have implications for the understanding of various complex metabolic pathways leading to disorders of the eye. The ultimate understanding leads to potential opportunities in evaluating miRNAs as molecular biomarkers, prognostic tools, diagnostic tools and therapeutic agents for eye disorders.
    Ophthalmic Research 03/2015; 53(4):169-186. DOI:10.1159/000371853
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    ABSTRACT: SIRT2 and SIRT6 are members of the sirtuin family and are associated with cancer development and progression in certain tumours, but their expression in retinoblastoma has not been studied. The primary objective of our study was to determine the expression of SIRT2 and SIRT6 in human retinoblastoma cases. Eighteen formalin-fixed paraffin-embedded blocks of retinoblastoma cases from the Ocular Pathology Registry at the Henry C. Witelson Ocular Pathology Laboratory were obtained, classified and immunostained for SIRT2 and SIRT6 using mouse monoclonal antibodies. Sixteen cases were poorly differentiated retinoblastoma cases. SIRT2 and SIRT6 were expressed in all cases of retinoblastoma although differences in the staining intensity were found between cases. SIRT2 and SIRT6 expression was also observed in various normal structures of the remaining ocular tissue. SIRT2 and SIRT6 are expressed in retinoblastoma, as well as in some normal ocular structures. While precise roles of these proteins must still be determined in retinoblastoma, their expression profiles suggest that further functional studies of both SIRT2 and SIRT6 should be pursued in this cancer. © 2015 S. Karger AG, Basel.
    Ophthalmic Research 01/2015; 53(2):100-8. DOI:10.1159/000368718
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    ABSTRACT: Purpose: The aim of this study was to investigate the effects of quercetin on vascular endothelial growth factor (VEGF)-induced choroidal and retinal angiogenesis in vitro using a rhesus macaque choroid-retinal endothelial (RF/6A) cell line. Methods: RF/6A cells were cultured in Dulbecco's modified Eagle's medium containing 10% fetal bovine serum. Then the cells were treated with different concentrations (from 0 to 100 μM) of quercetin and 100 ng/ml VEGF. The cell proliferation was assessed using cholecystokinin octapeptide dye. The cell migration was investigated by a Transwell assay. The tube formation was measured on Matrigel. Furthermore, the impact of quercetin's effects on VEGF-induced activation of VEGF receptor 2 (VEGFR-2) downstream signal pathways was tested by Western blot analysis. Results: Quercetin inhibits RF/6A cell proliferation in a dose-dependent fashion: 22.7, 31.5 and 36.7% inhibition on treatment with 10, 50 and 100 μM quercetin, respectively. VEGF-induced migration and tube formation of RF/6A cells were also significantly inhibited by quercetin in a dose-dependent manner. Quercetin inhibits VEGF-induced VEGFR-2 downstream signal pathways of RF/6A. Conclusions: The results show that quercetin inhibits VEGF-induced cell proliferation, migration and tube formation of RF/6A. We suggest that quercetin inhibits VEGF-induced choroidal and retinal angiogenesis in vitro. Collectively, the findings in the present study suggest that quercetin inhibits VEGF-induced choroidal and retinal angiogenesis by targeting the VEGFR-2 pathway. This suggests that quercetin is a choroidal and retinal angiogenesis inhibitor. © 2015 S. Karger AG, Basel.
    Ophthalmic Research 01/2015; 53(3):109-116. DOI:10.1159/000369824
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    ABSTRACT: Purpose: To evaluate the rotational stability of two intraocular lenses (IOLs) of similar design and material but with a difference of 1 mm in overall length. Methods: In this prospective study patients with age-related cataract were included. An IOL with an overall diameter of 12 mm (ACR6 = small-diameter IOL) was compared to an IOL with an overall diameter of 13 mm (IDEA 613 XC = large-diameter IOL). Results: In total, 60 patients were included in this study. Absolute rotation in the small- and large-diameter groups was 4.4° (SD: 4.0; range: 0.3-17.8) and 3.0° (SD: 2.4; range: 0.1-7.8), respectively. The differences between the two IOLs were not found to be statistically significant. Conclusion: The effect of the overall length of an IOL appears to have little impact on early rotation after cataract surgery. © 2015 S. Karger AG, Basel.
    Ophthalmic Research 01/2015; 53(3):117-121. DOI:10.1159/000368658
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    ABSTRACT: Objective: To report the clinical outcome of autologous cultured limbal epithelial cell transplantation (CLECT) followed by deep anterior lamellar keratoplasty (DALK) in paediatric eyes and to correlate the clinical outcome with the phenotype of rejuvenated corneal epithelium. Methods: Four patients with total limbal stem cell deficiency (LSCD) underwent autologous CLECT. Cultivated cell sheets were transplanted onto the damaged ocular surface followed by DALK surgery. Excised corneal buttons were subjected to histopathological analysis. Data recorded included age, sex, laterality, nature of injury, follow-up period, severity of stem cell deficiency, visual acuity, Schirmer's test and impression cytology. Results: At a mean follow-up period of 19.5 ± 7.4 (range 9-26) months after CLECT, all 4 eyes showed epithelialized and clinically stabilized ocular surface. Manual DALK was performed in all 4 eyes, with a mean follow-up of 9.75 ± 4.5 (range 5-15) months. All eyes exhibited smooth and clear corneal epithelium with improved visual acuity. Excised corneal buttons demonstrated organized corneal epithelial morphology and showed expression of cornea-specific CK3/12 marker. Conclusion: Restoration of severely damaged ocular surface following chemical injury by using 2-stage meticulous approaches offers a new modality for the treatment of severe LSCD. Transplantation of cultivated autologous limbal epithelial cell sheet followed by DALK surgery can efficiently restore the corneal phenotype with improved vision.
    Ophthalmic Research 06/2013; 50(1):59-64.
  • Ophthalmic Research 01/2013; 50(2):99-107.
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    ABSTRACT: To report detection of leprosy in ocular tissue by histopathology and its confirmation by genetic analysis. Excised tissue from a clinically-suspected ocular leprosy patient was processed and analyzed histopathologically. The DNA from the paraffin-embedded tissue was extracted, an 85 A-C intergenic region of Mycobacterium leprae was amplified using specific primers and analyzed by conventional as well as real-time polymerase chain reaction (RT-PCR). With periodic acid-Schiff-hematoxylin (PAS-H) staining the specimen showed presence of a thin fibrinous layer of inflammatory cells. The majority of the tissue was fibrovascular with extensive infiltration by histiocytes having reticulated cytoplasm. Modified PAS-H and acid-fast staining (AFS) showed the presence of several acid-fast organisms within the cytoplasm of histiocytes and mast cells. Conventional PCR showed a 250-bp DNA from excised conjunctival tissue, which was in agreement with the positive controls for M. leprae. Through RT-PCR, it was calculated that the suspected tissue had 44.68 pg of M. leprae DNA, which is 8937.06 genome copies of M. leprae. Presence of inflammatory cells and AFS bacilli in tissue presented a typical picture of leprosy. M. leprae DNA can be detected using RT-PCR in ocular tissues when acid-fast bacteria are seen in histopathological sections. And when the diagnosis of leprosy is inconclusive and acid-fast bacteria are seen, RT-PCR for M. leprae DNA could be used as a rapid confirmatory test to identify the presence of M. leprae and, therefore, the diagnosis of leprosy.
    Ophthalmic Research 02/2007; 39(2):63-8. DOI:10.1159/000099375
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    ABSTRACT: In glaucoma, retinal ganglion cell (RGC) death is induced by many risk factors, including ocular hypertension. It has been proposed that glutamate-mediated oxidative stress may also contribute to this RGC death. Cannabinoids are known to possess therapeutic properties including ocular hypotension and antioxidation. In this study, we test the hypothesis that (-)Delta(9)-tetrahydrocannabinol (THC) lowers intraocular pressure (IOP) and prevents RGC death in a rat model of glaucoma. Arat model of experimental glaucoma with chronic, moderately elevated IOP was produced unilaterally by cauterization of episcleral vessels. Rats received weekly injections of THC at a level of 5 mg/kg or vehicle for 20 weeks. IOP of both eyes was measured weekly on anesthetized animals immediately before THC treatment. RGCs were labeled in a retrograde fashion and counted in whole-mounted retinas. IOP was elevated in all operated eyes 1 day after the operation and remained elevated in the vehicle-treated rats throughout 20 weeks. In THC-treated rats, IOP elevation in operated eyes was diminished 2 weeks after operation and remained reduced. IOP in the contralateral control eyes was not affected by THC. In the operated eyes of vehicle-treated animals, there was a loss of approximately 50 and 40% of the RGCs in the peripheral and central retina, respectively. The RGC loss in the operated eyes of the THC-treated animals was reduced to 10-20%. These results demonstrate that THC is a neuroprotectant that preserves RGCs in an experimental model of glaucoma, possibly through a reduction in IOP.
    Ophthalmic Research 02/2007; 39(2):69-75. DOI:10.1159/000099240
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    ABSTRACT: To compare the efficacy ofa combination therapy of triamcinolone acetonide (TA) administration with and without vitrectomy in eyes with macular edema associated with branch retinal vein occlusion over a 1-year period. A retrospective, case-control study was conducted in 15 eyes of 15 patients with macular edema associated with branch retinal vein occlusion. Eight eyes underwent simultaneous intravitreal and posterior sub-Tenon capsule injections of TA (TA-injected group). Seven eyes underwent vitrectomy with intravitreal or simultaneous posterior sub-Tenon capsule injection of TA (vitrectomy with TA group). Macular thickness and visual acuity were measured before and at 1, 3, 6 and 12 months after the therapy. Twelve months after the therapy, mean visual acuity improved significantly from baseline in both the TA-injected (p = 0.0069) and vitrectomy with TA groups (p = 0.0145). Macular thickness also improved significantly in both the TA-injected (p = 0.0065) and vitrectomy with TA groups (p = 0.0058). At 12 months after the therapy, there was no significant difference in visual acuity and macular thickness between the two groups (p = 0.3308 and 0.3711, respectively). At the early postoperative stage (1 and 3 months after the therapy), the central macular thickness in the TA-injected group was significantly less than that in the vitrectomy with TA group (p = 0.0140 and 0.0275, respectively); there was no significant difference in visual acuity between the two groups (p = 0.0796 and 0.3753, respectively). TA injection without vitrectomy was as effective as a combination therapy of TA injection with vitrectomy.
    Ophthalmic Research 02/2007; 39(4):207-12. DOI:10.1159/000104682
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    ABSTRACT: The immunohistochemical expressions of two multidrug resistance proteins, P-glycoprotein (P-gp) and multidrug resistance-related protein-1 (MRP-1), were studied in retinoblastoma and the correlations with the clinicopathological parameters were assessed. Sixty-five enucleated eyes containing retinoblastoma were included in the study. Following hematoxylin-eosin staining, tumor differentiation, presence of choroidal invasion, optic nerve invasion, retinal invasion, necrosis and presence of calcification were evaluated with the light microscope. P-gp and MRP-1 expressions were evaluated immunohistochemically. Fifty-three eyes were enucleated primarily and 12 eyes were operated after failure of chemotherapy. P-gp and MRP-1 expressions were positive in 69.3 and 73.4% of specimens, respectively. There was no statistically significant relationship between the expressions of P-gp and MRP-1, and tumor differentiation, presence of tumor invasion or treatment with chemotherapy. Retinoblastoma intrinsically expresses both P-gp and MRP-1 and their expressions are not related to tumor differentiation. The expressions of P-gp and MRP-1 do not seem to be induced by chemotherapy and are not related to the degree of tumor invasion.
    Ophthalmic Research 02/2007; 39(4):191-7. DOI:10.1159/000104680
  • Ophthalmic Research 02/2007; 39(2):62. DOI:10.1159/000099239
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    ABSTRACT: Mutations and polymorphisms have been identified in the CYP1B1 gene; while mutations that affect the conserved core structures of cytochrome P4501B1 result in primary congenital glaucoma (PCG), mutations in other regions hold the potential to define differences in estrogen metabolism. In the present study, we analyzed the CYP1B1 gene in Mexican patients with PCG and described four novel mutations. The sample included 12 nonrelated cases with PCG. Analysis of coding regions of the CYP1B1 gene was performed through PCR and DNA sequencing analysis from genomic DNA. Molecular analysis of the CYP1B1 gene showed the following molecular defects: (1) a novel single-base pair deletion within codon 370 (1454delC) that produces a substitution of leucine instead of proline and a premature stop codon 57 amino acids after the last original amino acid; this family also harbored a novel polymorphic variant of the cytochrome P4501B1 with six single-nucleotide polymorphisms (142C-->G; 355G-->T; 729G-->C; 4326C-->G; 4360C-->G and 4379C-->T); (2) a novel single-base pair deletion within codon 277 (1176delT) that results in a premature stop codon; (3) a novel single-base pair deletion within codon 179 (880delG) that produces a substitution of arginine instead of alanine and a premature stop codon 17 amino acids downstream from the last original amino acid, and (4) a duplication (or insertion) of ten base pairs within codon 404 (1556dupATGCCACCAC) that results in a premature stop codon 26 amino acids after the last original amino acid. We also observed in 2 nonrelated patients a deletion of 13 bp (1410_1422delGAGTGCAGGCAGA) previously reported for other populations. We reported four novel mutations and a novel polymorphic variant in the CYP1B1 gene in PCG in the Mexican population; it has important implications in diagnosis and genetic counseling.
    Ophthalmic Research 02/2007; 39(1):17-23. DOI:10.1159/000097902
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    ABSTRACT: RhoA is a small guanosine triphosphatase which participates in signaling pathways of axonal repellents or inhibitors. However, the distribution and expression of RhoA in the rat retina after optic nerve injury has not been elucidated yet. To study the distribution and expression of RhoA in the rat retina after optic nerve injury. Immunohistochemistry was used to determine the distribution of RhoA in rat retina after optic nerve injury. The expression of RhoA was analyzed by Western blot. In normal retina and the retina 1 day after optic nerve injury, RhoA was distributed in the retinal ganglion cell (RGC) layer. Three days after optic nerve injury, it existed in RGCs and the inner plexiform layer. However, 7 days after surgery its immunoreactivity was abundant not only in the RGC and inner plexiform layers but also in the inner nuclear and outer plexiform layers. Western blot analysis showed that the expression of RhoA increased significantly in the retina after optic nerve injury in comparison with normal retina. These results indicate that the distribution and expression of RhoA were extended and enhanced after optic nerve injury, and that RhoA plays an important role in optic nerve regeneration.
    Ophthalmic Research 02/2007; 39(3):174-8. DOI:10.1159/000103237
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    ABSTRACT: Retinoblastoma is the most common cancer of the eye in children and is uniformly fatal if left untreated. Over the past century, there have been great strides in treatment that have resulted in survival rates greater than 95% in developed countries [1]. However, currently available treatments have serious drawbacks, and many retinoblastoma-bearing eyes continue to require enucleation. External beam radiotherapy, while highly effective in many cases, markedly increases the risk of second primary cancers in the field of radiation in young children with the heritable form of retinoblastoma, which represents about 40% of all cases [2]. Even in nonheritable cases, radiation can induce disfiguring midfacial hypoplasia. Because of these shortcomings, external beam radiotherapy has been largely replaced by systemic chemotherapy – usually a combination of carboplatin, vincristine and etoposide [3, 4]. When combined with focal laser treatment and cryotherapy, chemotherapy allows many eyes to be salvaged without external radiation. Indeed, the success of combination chemotherapy and focal treatment has spurred the development of a new international classification for intraocular retinoblastoma based on systemic chemotherapy. Nevertheless, chemotherapy has its own drawbacks, including bone marrow suppression, infections and possibly second cancers such as leukemia. In addition, chemotherapy has done little to reduce the need for enucleation in eyes with advanced disease. Sadly, many children with advanced ‘group D’ disease end up being treated with external beam radiotherapy after a full course of chemotherapy has failed, thereby exposing them to the risks of both therapies. Thus, despite many successes in treating retinoblastoma, there is still a long way to go.
    Ophthalmic Research 02/2007; 39(4):188-90. DOI:10.1159/000103578
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    ABSTRACT: To investigate the role played by E26 transformation-specific-1 (Ets-1), a transcription factor, and extracellular signal-regulated kinase 1/2 (ERK1/2) in the expression of vascular endothelial growth factor (VEGF), and the interaction of Ets-1 and ERK1/2 in the retina of diabetic rats. Diabetes was induced in rats by an intraperitoneal injection of streptozotocin (STZ). To follow the time course in the expression of Ets-1, phosphorylated ERK1/2 (pERK1/2), and VEGF, rats were killed at 1, 2, 4, and 8 weeks after the injection of STZ, and total proteins were extracted from the isolated retinas. An adenovirus vector encoding dominant-negative Ets-1 and an inhibitor of PD98059 was injected intravitreally to investigate the effects of Ets-1 blockade and ERK1/2 inhibition on the expression of VEGF. Four weeks after the first intravitreal injection, total proteins and total RNA were extracted from the retinas for Western blot and Northern blot analyses. The expression of Ets-1, pERK1/2, and VEGF in the retina increased in a time-dependent manner after STZ injection. The phosphorylation of ERK1/2 and protein level of VEGF were significantly reduced following intravitreal Ets-1. Inhibition of ERK1/2 phosphorylation resulted in a significant reduction in the expression of Ets-1 and the level of VEGF protein. These results indicate that in the retina of STZ-induced diabetic rats: (1) the alterations of Ets-1, pERK1/2, and VEGF are approximately synchronized; (2) the phosphorylation of ERK1/2 is regulated by the expression of Ets-1; (3) the production of Ets-1 protein is dependent on the ERK1/2 pathway, and (4) the protein level of VEGF is regulated by both Ets-1 expression and ERK1/2 phosphorylation. We propose that VEGF, Ets-1, and ERK1 act synergistically in the development of diabetic retinopathy.
    Ophthalmic Research 02/2007; 39(4):224-31. DOI:10.1159/000104831