Bromfenac sodium 0.1%, fluorometholone 0.1% and dexamethasone 0.1% for control of ocular inflammation and prevention of cystoid macular edema after phacoemulsification.

PURPOSE: To compare bromfenac sodium 0.1%, fluorometholone 0.1% and dexamethasone 0.1% for the control of postoperative inflammation and prevention of cystoid macular edema (CME) after phacoemulsification. METHODS: Patients were randomized to receive bromfenac sodium 0.1% for 1 month (OBS1) or 2 months (OBS2), or fluorometholone 0.1% for 1 month (OFM) or dexamethasone 0.1% for 1 month (ODM). Best-corrected visual acuity, intraocular pressure, endothelial cell density, photon count value and retinal foveal thickness were measured. RESULTS: Mean photon count values were lower in the OBS1 and OBS2 groups compared with the ODM group during the first week. Bromfenac sodium cleared the ocular inflammation more rapidly than fluorometholone and dexamethasone. The foveal thickness was thinner in the second month and the incidence of CME was lower in the OBS1 and OBS2 groups compared with the OFM and ODM groups. CONCLUSION: Bromfenac sodium was more effective and safer than fluorometholone and dexamethasone as an anti-inflammatory, decreasing macular thickness and preventing CME in age-related cataract patients after cataract surgery.

[Clinical evaluation on the coaxial 1.8 mm microincision cataract surgery].

OBJECTIVE: To study and compare the outcomes of coaxial 1.8 mm microincision phacoemulsification with conventional coaxial 3 mm small-incision cataract surgery. METHODS: A randomized prospective study was conducted on 89 patients with age-related cataract: coaxial 1.8 mm microincision cataract surgery (MICS group) was performed in 45 cases (45 eyes), and coaxial 3 mm small-incision cataract surgery (SICS group) was performed in 44 cases (44 eyes). Statistical analysis was taken with the data of 40 cases (40 eyes) in the MICS group and 40 cases (40 eyes) in the SICS group. The average ultrasound power (AVE) and effective phacoemulsification time (EPT) were recorded during the operation. Visual acuity, endothelial cell density and cornea thickness were compared at intervals of 1 day, 1 week, 1 month and 3 months after surgery. In addition, surgically induced astigmatism (SIA) was analyzed. Statistic analysis was taken by student's t test and chi square test. RESULTS: There was no significant difference on AVE and EPT (P > 0.05) between these two groups. One day after the surgery, the MICS group showed better uncorrected visual acuity (0.16 ± 0.14) as compared to the SICS group (0.23 ± 0.12). The difference was statistically significant (P < 0.05). There were no significant differences on best corrected visual acuity, endothelial cell density and cornea thickness between these two groups. One week, 1 month and 3 months after the surgery, SIA was (0.62 ± 0.28) D, (0.48 ± 0.28) D, (0.47 ± 0.25) D, (0.40 ± 0.24) D in the MICS group, and (1.27 ± 0.65) D, (1.18 ± 0.59) D, (1.02 ± 0.56) D, (0.79 ± 0.48) D in the SICS group, respectively. The differences between the MIC and SICS groups were statistically significant (P < 0.01). SIA decreased significantly and became stable 1 week after surgery in MICS group, while the similar tendency appeared one month after the surgery in the SICS group. CONCLUSIONS: Coaxial 1.8 mm microincision cataract surgery could significantly reduce SIA and obtain more stable astigmatism status. This suggests that the coaxial MICS phacoemulsification surgery could get earlier visual rehabilitation postoperatively.

[Computer construction and analysis of protein models of mutant fibrillin-1 gene in Marfan's syndrome].

OBJECTIVE: Fibrillin-1, the major constituent of extracellular microfibrils, plays an important role in the molecular pathogenesis of Marfan syndrome (MFS, #54700). The aim of this study was to analyze protein models of the mutation of the fibrillin-1 (FBN1) gene on Arg545Cys and Arg1530Cys which have been reported to cause predominant ectopia lentis in Chinese patients. METHODS: We constructed and analyzed the protein models of the mutant FBN1 gene on Arg545Cys and Arg1530Cys. Fibrillin-1 protein structures were predicted by SWISS-MODEL. Models were viewed in Swiss-Pdb Viewer. RESULTS: Computer construction and analysis of protein models of the mutant FBN1 gene revealed that the mutant Arg545Cys FBN1 protein had various changes on protein's secondary structure with an absence of a helix, decreased hydrogen bond distance, different protein surface solvent-accessibility and decreased negative electrostatic potential. The mutant Arg1530Cys FBN1 showed lost of hydrogen bonds, different protein surface solvent-accessibility and increased negative electrostatic potential. CONCLUSIONS: Protein models of the mutant FBN1 gene shows significant alterations on the protein's secondary structure based on computer construction and analysis technology. This study provides further evidence for the important effect of the mutant FBN1 on the pathogenesis of human ectopia lentis.

Identification of a novel frameshift mutation in PITX2 gene in a Chinese family with Axenfeld-Rieger syndrome.

OBJECTIVE: Axenfeld-Rieger syndrome (ARS) is phenotypically and genetically heterogeneous. In this study, we identified the underlying genetic defect in a Chinese family with ARS. METHODS: A detailed family history and clinical data were recorded. The ocular phenotype was documented using slit-lamp photography and systemic anomalies were also documented where available. The genomic DNA was extracted from peripheral blood leukocytes. All coding exons and intron-exon junctions of paired-like homeodomain transcription factor 2 (PITX2) gene and the forkhead box C1 (FOXC1) gene were amplified by polymerase chain reaction (PCR) and screened for mutation by direct DNA sequencing. Variations detected in exon 5 of PITX2 were further evaluated with cloning sequencing. The exon 5 of PITX2 was also sequenced in 100 healthy controls, unrelated to the family, for comparison. Structural models of the wild type and mutant homeodomain of PITX2 were investigated by SWISS-MODEL. RESULTS: Affected individuals exhibited variable ocular phenotypes, whereas the systemic anomalies were similar. After direct sequencing and cloning sequencing, a heterozygous deletion/insertion mutation c.198_201delinsTTTCT (p.M66Ifs*133) was revealed in exon 5 of PITX2. This mutation co-segregated with all affected individuals in the family and was not found either in unaffected family members or in 100 unrelated controls. CONCLUSIONS: We detected a novel frameshift mutation p.M66Ifs*133 in PITX2 in a Chinese family with ARS. Although PITX2 mutations and polymorphisms have been reported from various ethnic groups, we report for the first time the identification of a novel deletion/insertion mutation that causes frameshift mutation in the homeodomain of PITX2 protein.