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Biomedical subjects

David M Brown

Publications and source records attributed to David M Brown.

18 recordsLinked to original sources

Relationship between optical coherence tomography-measured central retinal thickness and visual acuity in diabetic macular edema.

OBJECTIVE: To compare optical coherence tomography (OCT)-measured retinal thickness and visual acuity in eyes with diabetic macular edema (DME) both before and after macular laser photocoagulation. DESIGN: Cross-sectional and longitudinal study. PARTICIPANTS: Two hundred ten patients (251 eyes) with DME enrolled in a randomized clinical trial of laser techniques. METHODS: Retinal thickness was measured with OCT and visual acuity was measured with the electronic Early Treatment of Diabetic Retinopathy procedure. MAIN OUTCOME MEASURES: Optical coherence tomography-measured center point thickness and visual acuity. RESULTS: The correlation coefficients for visual acuity versus OCT center point thickness were 0.52 at baseline and 0.49, 0.36, and 0.38 at 3.5, 8, and 12 months after laser photocoagulation. The slope of the best fit line to the baseline data was approximately 4.4 letters (95% confidence interval, 3.5-5.3) of better of visual acuity for every 100-mum decrease in center point thickness at baseline with no important difference at follow-up visits. Approximately one third of the variation in visual acuity could be predicted by a linear regression model that incorporated OCT center point thickness, age, hemoglobin A1C, and severity of fluorescein leakage. The correlation between change in visual acuity and change in OCT center point thickening 3.5 months after laser treatment was 0.44, with no important difference at the other follow-up times. A subset of eyes showed paradoxical improvements in visual acuity with increased center point thickening (7%-17% at the 3 time points) or paradoxical worsening of visual acuity with a decrease in center point thickening (18%-26% at the 3 time points). CONCLUSIONS: There is modest correlation between OCT-measured center point thickness and visual acuity, and modest correlation of changes in retinal thickening and visual acuity after focal laser treatment for DME. However, a wide range of visual acuity may be observed for a given degree of retinal edema. Thus, although OCT measurements of retinal thickness represent an important tool in clinical evaluation, they cannot substitute reliably as a surrogate for visual acuity at a given point in time. This study does not address whether short-term changes on OCT are predictive of long-term effects on visual acuity.

Diabetic Retinopathy↗

Binary and ternary complexes containing alpha-cyclodextrin and bromonaphthalene derivatives: a note of caution in interpreting UV absorption spectral data.

Ultraviolet absorption spectra, NMR spectra, and phosphorescence measurements were used to confirm that alpha-cyclodextrin (CD) and 2-bromo-6-beta-D-glucopyranosidylnaphthalene (BGN) form only a binary complex and to characterize its properties. The binding constant for the CD.BGN complex was found to be 886 +/- 24 M(-1) and 770 +/- 110 M(-1) from NMR and UV absorbance measurements, respectively. Comparison of spectral properties revealed the CD.BGN complex to be binary and complexes containing CD and n-alkoxy (n-alkanoloxy) derivatives of 2-bromonaphthalene (N) to be of higher order, notably ternary. A red shift was observed in the UV absorption spectra of the CD(2).N complexes. The absence of a hydroxyl hydrogen atom on the naphthalene ring of N molecules made it impossible for hydrogen bond formation to a glucosidic oxygen in the CD cavity to be the cause of the red shift. The similar red shifts reported herein and for the ternary complexes of CD with 2-naphthol and 2-bromo-6-hydroxynaphthalene (BOHN) indicated that hydrogen bond formation between the hydroxyl hydrogen and glucosidic oxygen atom might not be the cause of the red shift for the latter guest molecules, as has been proposed previously. This result emphasizes the caution necessary in using UV absorption spectral data as evidence for hydrogen bond formation in molecular complexes containing CD.

Journal Article↗

Ranibizumab for neovascular age-related macular degeneration.

BACKGROUND: Ranibizumab--a recombinant, humanized, monoclonal antibody Fab that neutralizes all active forms of vascular endothelial growth factor A--has been evaluated for the treatment of neovascular age-related macular degeneration. METHODS: In this multicenter, 2-year, double-blind, sham-controlled study, we randomly assigned patients with age-related macular degeneration with either minimally classic or occult (with no classic lesions) choroidal neovascularization to receive 24 monthly intravitreal injections of ranibizumab (either 0.3 mg or 0.5 mg) or sham injections. The primary end point was the proportion of patients losing fewer than 15 letters from baseline visual acuity at 12 months. RESULTS: We enrolled 716 patients in the study. At 12 months, 94.5% of the group given 0.3 mg of ranibizumab and 94.6% of those given 0.5 mg lost fewer than 15 letters, as compared with 62.2% of patients receiving sham injections (P<0.001 for both comparisons). Visual acuity improved by 15 or more letters in 24.8% of the 0.3-mg group and 33.8% of the 0.5-mg group, as compared with 5.0% of the sham-injection group (P<0.001 for both doses). Mean increases in visual acuity were 6.5 letters in the 0.3-mg group and 7.2 letters in the 0.5-mg group, as compared with a decrease of 10.4 letters in the sham-injection group (P<0.001 for both comparisons). The benefit in visual acuity was maintained at 24 months. During 24 months, presumed endophthalmitis was identified in five patients (1.0%) and serious uveitis in six patients (1.3%) given ranibizumab. CONCLUSIONS: Intravitreal administration of ranibizumab for 2 years prevented vision loss and improved mean visual acuity, with low rates of serious adverse events, in patients with minimally classic or occult (with no classic lesions) choroidal neovascularization secondary to age-related macular degeneration. (ClinicalTrials.gov number, NCT00056836 [ClinicalTrials.gov].).

Aged↗

Ranibizumab versus verteporfin for neovascular age-related macular degeneration.

BACKGROUND: We compared ranibizumab--a recombinant, humanized, monoclonal antibody Fab that neutralizes all active forms of vascular endothelial growth factor A--with photodynamic therapy with verteporfin in the treatment of predominantly classic neovascular age-related macular degeneration. METHODS: During the first year of this 2-year, multicenter, double-blind study, we randomly assigned patients in a 1:1:1 ratio to receive monthly intravitreal injections of ranibizumab (0.3 mg or 0.5 mg) plus sham verteporfin therapy or monthly sham injections plus active verteporfin therapy. The primary end point was the proportion of patients losing fewer than 15 letters from baseline visual acuity at 12 months. RESULTS: Of the 423 patients enrolled, 94.3% of those given 0.3 mg of ranibizumab and 96.4% of those given 0.5 mg lost fewer than 15 letters, as compared with 64.3% of those in the verteporfin group (P<0.001 for each comparison). Visual acuity improved by 15 letters or more in 35.7% of the 0.3-mg group and 40.3% of the 0.5-mg group, as compared with 5.6% of the verteporfin group (P<0.001 for each comparison). Mean visual acuity increased by 8.5 letters in the 0.3-mg group and 11.3 letters in the 0.5-mg group, as compared with a decrease of 9.5 letters in the verteporfin group (P<0.001 for each comparison). Among 140 patients treated with 0.5 mg of ranibizumab, presumed endophthalmitis occurred in 2 patients (1.4%) and serious uveitis in 1 (0.7%). CONCLUSIONS: Ranibizumab was superior to verteporfin as intravitreal treatment of predominantly classic neovascular age-related macular degeneration, with low rates of serious ocular adverse events. Treatment improved visual acuity on average at 1 year. (ClinicalTrials.gov number, NCT00061594 [ClinicalTrials.gov].).

Aged↗

Prospective study of changes in bone mineral density and turnover in children after hematopoietic cell transplantation.

CONTEXT: Osteoporosis is common in adults after hematopoietic cell transplantation (HCT). The data on bone mineral density (BMD) in children after HCT are limited. OBJECTIVE: The objective of the study was to determine the incidence, timing, magnitude, and possible predictors of bone loss in children after HCT. PATIENTS AND DESIGN: The study population included 49 patients (age 5-18 yr) who were eligible to receive HCT at the University of Minnesota. The patients were evaluated at baseline, 100 d, 6 months, and 1 yr after HCT. Lumbar BMD (LBMD) was assessed by dual-energy x-ray absorptiometry. RESULTS: The number of patients with osteopenia increased from 18% at baseline to 33% 1 yr after HCT, and with osteoporosis from 16-19%. Mean areal LBMD z-score decreased from -0.56 to -1.1 by 6 months (n = 27) and at 1 yr was -0.94 (n = 21), which was significant compared with standard normal distribution (P = 0.004 and P = 0.022, respectively). The absolute loss of bone mineral corresponded to a 5.3% reduction in areal LBMD and a 4.8% reduction in volumetric LBMD. The level of bone-specific alkaline phosphatase decreased by 30% by d 100 (P = 0.009), followed by recovery toward baseline by 6 months. The level of osteocalcin greater than 6.5 ng/ml at d 100 predicted recovery from the initial bone loss by 1 yr. A reduction in LBMD at 6 months correlated with a cumulative dose of glucocorticoids. CONCLUSION: This study demonstrates that bone loss is common in children after HCT and is primarily due to suppression of bone formation. Further studies are necessary to validate osteocalcin as a predictive biomarker.

Absorptiometry, Photon↗

Ultrafine particles cause cytoskeletal dysfunctions in macrophages: role of intracellular calcium.

BACKGROUND: Particulate air pollution is reported to cause adverse health effects in susceptible individuals. Since most of these particles are derived form combustion processes, the primary composition product is carbon with a very small diameter (ultrafine, less than 100 nm in diameter). Besides the induction of reactive oxygen species and inflammation, ultrafine particles (UFP) can cause intracellular calcium transients and suppression of defense mechanisms of alveolar macrophages, such as impaired migration or phagocytosis. METHODS: In this study the role of intracellular calcium transients caused by UFP was studied on cytoskeleton related functions in J774A.1 macrophages. Different types of fine and ultrafine carbon black particles (CB and ufCB, respectively), such as elemental carbon (EC90), commercial carbon (Printex 90), diesel particulate matter (DEP) and urban dust (UD), were investigated. Phagosome transport mechanisms and mechanical cytoskeletal integrity were studied by cytomagnetometry and cell viability was studied by fluorescence microscopy. Macrophages were exposed in vitro with 100 and 320 microg UFP/ml/million cells for 4 hours in serum free medium. Calcium antagonists Verapamil, BAPTA-AM and W-7 were used to block calcium channels in the membrane, to chelate intracellular calcium or to inhibit the calmodulin signaling pathways, respectively. RESULTS: Impaired phagosome transport and increased cytoskeletal stiffness occurred at EC90 and P90 concentrations of 100 microg/ml/million cells and above, but not with DEP or UD. Verapamil and W-7, but not BAPTA-AM inhibited the cytoskeletal dysfunctions caused by EC90 or P90. Additionally the presence of 5% serum or 1% bovine serum albumin (BSA) suppressed the cytoskeletal dysfunctions. Cell viability showed similar results, where co-culture of ufCB together with Verapamil, W-7, FCS or BSA produced less cell dead compared to the particles only.

Journal Article↗

Identification of novel genes in Arabidopsis involved in secondary cell wall formation using expression profiling and reverse genetics.

Forward genetic screens have led to the isolation of several genes involved in secondary cell wall formation. A variety of evidence, however, suggests that the list of genes identified is not exhaustive. To address this problem, microarray data have been generated from tissue undergoing secondary cell wall formation and used to identify genes that exhibit a similar expression pattern to the secondary cell wall-specific cellulose synthase genes IRREGULAR XYLEM1 (IRX1) and IRX3. Cross-referencing this analysis with publicly available microarray data resulted in the selection of 16 genes for reverse genetic analysis. Lines containing an insertion in seven of these genes exhibited a clear irx phenotype characteristic of a secondary cell wall defect. Only one line, containing an insertion in a member of the COBRA gene family, exhibited a large decrease in cellulose content. Five of the genes identified as being essential for secondary cell wall biosynthesis have not been previously characterized. These genes are likely to define entirely novel processes in secondary cell wall formation and illustrate the success of combining expression data with reverse genetics to address gene function.

3' Untranslated Regions↗

The effect of refurbishing a UK steel plant on PM10 metal composition and ability to induce inflammation.

BACKGROUND: In the year 2000 Corus closed its steel plant operations in Redcar, NE of England temporarily for refurbishment of its blast furnace. This study investigates the impact of the closure on the chemical composition and biological activity of PM10 collected in the vicinity of the steel plant. METHODS: The metal content of PM10 samples collected before during and after the closure was measured by ICP-MS in order to ascertain whether there was any significant alteration in PM10 composition during the steel plant closure. Biological activity was assessed by instillation of 24 hr PM10 samples into male Wistar rats for 18 hr (n = 6). Inflammation was identified by the cellular and biochemical profile of the bronchoalveolar lavage fluid. Metal chelation of PM10 samples was conducted using Chelex beads prior to treatment of macrophage cell line, J774, in vitro and assessment of pro-inflammatory cytokine expression. RESULTS: The total metal content of PM10 collected before and during the closure period were similar, but on reopening of the steel plant there was a significant 3-fold increase (p < 0.05) compared with the closure and pre-closure samples. Wind direction prior to the closure was predominantly from the north, compared to south westerly during the closure and re-opened periods. Of metals analysed, iron was most abundant in the total and acid extract, while zinc was the most prevalent metal in the water-soluble fraction. Elevated markers of inflammation included a significant increase (p < 0.01) in neutrophil cell numbers in the bronchoalveolar lavage of rats instilled with PM10 collected during the reopened period, as well as significant increases in albumin (p < 0.05). Extracts of PM10 from the pre-closure and closure periods did not induce any significant alterations in inflammation or lung damage. The soluble and insoluble extractable PM10 components washed from the reopened period both induced a significant increase in neutrophil cell number (p < 0.05) when compared to the control, and these increases when added together approximately equalled the inflammation induced by the whole sample. PM10 from the re-opened period stimulated J774 macrophages to generate TNF-alpha protein and this was significantly prevented by chelating the metal content of the PM10 prior to addition to the cells. CONCLUSION: PM10-induced inflammation in the rat lung was related to the concentration of metals in the PM10 samples tested, and activity was found in both the soluble and insoluble fractions of the particulate pollutant.

Air Pollutants↗

An authentic 3' noncoding region is necessary for efficient poliovirus replication.

Picornavirus RNA replication involves the specific synthesis of negative-strand intermediates followed by an accumulation of positive-strand viral RNA in the presence of a multitude of cellular mRNAs. Previously, in an effort to identify cis-acting elements required for initiation of negative-strand RNA synthesis, we deleted the entire 3' noncoding regions from human rhinovirus and poliovirus genomic RNAs. These deletion mutation transcripts displayed a severe delay in RNA accumulation following transfection of HeLa cells. Interestingly, in subsequent infection of HeLa cells, the deletion-mutant poliovirus displayed only a moderate deficiency in RNA synthesis. These data suggested that the delay in the production of cytopathic effects after transfection may have been due to an RNA replication defect overcome by the accumulation of a compensatory mutation(s) generated during initial rounds of RNA synthesis. In this study, we have sequenced the entire genome of the deletion-mutant virus and found only two nucleotide changes from the parental clone. Transfection analysis of these sequence variants revealed that the sequence changes did not provide compensatory functions for the 3' noncoding region deletion mutation replication defect. Further examination of the deletion mutant phenotype revealed that the severe replication defect following RNA transfection is due, in part, to nonviral terminal sequences present in the in vitro-derived deletion mutation transcripts. Our data suggest that poliovirus RNA harboring a complete 3' noncoding region deletion mutation is infectious (not merely quasi-infectious).

3' Untranslated Regions↗

Flavonoid compounds in maintenance of prostate health and prevention and treatment of cancer.

Compounds based on a flavonoid (di-phenolic) ring structure are emerging as a potentially important new class of pharmaceutical compounds with a broad range of biological activities, most prominent of which are their potential role as anticancer agents. These compounds exert a wide range of upregulating and downregulating effects on signal transduction processes within cells in both plants and animals. The observation that human communities, which consume large quantities of these compounds (legume-based vegetarian diets), have a lower incidence of many degenerative diseases and some cancers has led to the speculation that these compounds, or synthetic analogs, may be of therapeutic value. This article reviews the evidence supporting this hypothesis and provides some examples of attempts to develop new therapeutics based on dietary isoflavones or novel isoflavonoid structures in maintaining prostate health and in cancer treatment and management. One of these compounds, phenoxodiol, is now in human clinical trials and has shown promise in patients with recurrent ovarian cancer where the cancer is refractory or resistant to standard chemotherapy, and in patients with hormone-refractory prostate cancer.

Animals↗

Cell-dependent role for the poliovirus 3' noncoding region in positive-strand RNA synthesis.

We previously reported the isolation of a mutant poliovirus lacking the entire genomic RNA 3' noncoding region. Infection of HeLa cell monolayers with this deletion mutant revealed only a minor defect in the levels of viral RNA replication. To further analyze the consequences of the genomic 3' noncoding region deletion, we examined viral RNA replication in a neuroblastoma cell line, SK-N-SH cells. The minor genomic RNA replication defect in HeLa cells was significantly exacerbated in the SK-N-SH cells, resulting in a decreased capacity for mutant virus growth. Analysis of the nature of the RNA replication deficiency revealed that deleting the poliovirus genomic 3' noncoding region resulted in a positive-strand RNA synthesis defect. The RNA replication deficiency in SK-N-SH cells was not due to a major defect in viral translation or viral protein processing. Neurovirulence of the mutant virus was determined in a transgenic mouse line expressing the human poliovirus receptor. Greater than 1,000 times more mutant virus was required to paralyze 50% of inoculated mice, compared to that with wild-type virus. These data suggest that, together with a cellular factor(s) that is limiting in neuronal cells, the poliovirus 3' noncoding region is involved in positive-strand synthesis during genome replication.

3' Untranslated Regions↗

Functional conservation of the hydrophobic domain of polypeptide 3AB between human rhinovirus and poliovirus.

In this study we exchanged portions of the poliovirus type 1 (PV1) hydrophobic domain within the membrane-associated polypeptide 3AB for the analogous sequences from human rhinovirus 14 (HRV14). The sequence exchanges were based upon a previous report in which the 22 amino acid hydrophobic region was subdivided into two domains, I and II, the latter of which was shown to be required for membrane association (J. Biol. Chem. 271 (1996), 26810). Using these divisions, the HRV14 sequences were cloned into the complete poliovirus type 1 cDNA sequence. RNAs transcribed from these cDNAs were transfected into HeLa cell monolayers and used in HeLa cell-free translation/replication assays. The data indicated that 3AB sequences from PV1 and HRV14 are interchangeable; however, the substitutions cause a range of significant RNA replication defects, and in some cases, protein processing defects. Following transfection of RNAs encoding the domain substitutions into HeLa cell monolayers, virus isolates were harvested, and the corresponding viral RNAs were sequenced. The sequence data revealed that for the carboxy-terminal domain substitutions (domain II), multiple nucleotide changes were identified in the first, second, and third positions of different codons. In addition, the data indicated that for one of the PV1/HRV14 chimeras to replicate, compensatory mutations within poliovirus protein 2B may be required.

Amino Acid Sequence↗

Oxidative stress and calcium signaling in the adverse effects of environmental particles (PM10).

This review focuses on the potential role that oxidative stress plays in the adverse effects of PM(10). The central hypothesis is that the ability of PM(10) to cause oxidative stress underlies the association between increased exposure to PM(10) and both exacerbations of lung disease and lung cancer. Pulmonary inflammation may also underlie the cardiovascular effects seen following increased PM(10), although the mechanisms of the cardiovascular effects of PM(10) are not well understood. PM(10) is a complex mix of various particle types and several of the components of PM(10) are likely to be involved in the induction of oxidative stress. The most likely of these are transition metals, ultrafine particle surfaces, and organic compounds. In support of this hypothesis, oxidative stress arising from PM(10) has been shown to activate a number of redox-responsive signaling pathways in lung target cells. These pathways are involved in expression of genes that play a role in responses relevant to inflammation and pathological change, including MAPKs, NF-kappaB, AP-1, and histone acetylation. Oxidative stress from particles is also likely to play an important role in the carcinogenic effects associated with PM(10) and hydroxyl radicals from PM(10) cause DNA damage in vitro.

Animals↗

The role of free radicals in the toxic and inflammatory effects of four different ultrafine particle types.

PM10 contains an ultrafine component, which is generally derived from combustion processes. This ultrafine fraction may be a factor in the increases in exacerbations of respiratory disease and deaths from cardiorespiratory causes associated with transient increases in levels of PM10. By using four different ultrafine particles (carbon black, cobalt, nickel, and titanium dioxide), we set out to determine the attributes of the ultrafine particle (surface area, chemical composition, particle number, or surface reactivity) that contribute most to its toxicity and proinflammatory effects both in vivo and in vitro. Instillation of 125 micro g ultrafine carbon black (UFCB) and ultrafine cobalt (UFCo) particles induced a significant influx of neutrophils at both 4 and 18 h postinstillation. Accompanying the influx of neutrophils was an increase in macrophage inflammatory protein-2 (MIP-2) (at 4 h) and an increase in gamma-glutamyl transpeptidase (at 18 h) in bronchoalveolar lavage fluid (BAL). Ultrafine nickel (UFNi) did not induce a significant increase in neutrophil influx until 18 h postinstillation. The increase in neutrophils induced by UFNi at this timepoint was comparable to that induced by UFCo and UFCB. UFTi did not induce a significant increase in neutrophils following instillation into the rat lung. The levels of MIP-2 observed at 4 h and neutrophil influx at 18 h induced by the particle samples were consistent with the pattern of surface free radical generation (as measured by the plasmid scission assay) whereby UFCo, UFCB, and UFNi all cause significant increases in inflammatory markers, as well as inducing a significant depletion of supercoiled plasmid DNA, indicative of hydroxyl radical generation. A role for free radicals and reactive oxygen species (ROS) in mediating ultrafine inflammation is further strengthened by the ability of the antioxidants N-acetylcysteine (NAC) and glutathione monoethyl ester (GSHme) to block the particle induced release of tumour necrosis factor-alpha (TNF-alpha) from alveolar macrophages in vitro. The ultrafine particles in PM10 may cause adverse effects via oxidative stress, and this could have implications for susceptible individuals. Susceptible individuals, such as those with COPD or asthma, already exhibit preexisting oxidative stress and hence are in a primed state for further oxidative stress induced by occupational or environmental particles.

Air Pollutants↗

New malaria chemotherapy developed by utilization of a unique parasite transport system.

During its development in the host red cell, the human malarial parasite causes profound alteration in the permeability of the host cell membrane. These membrane transport systems(s) play a role in the development of the intra-erythrocytic parasite in its need to take up solutes and nutrients from the extracellular medium and the disposal of metabolic wastes. Importantly, the properties of these parasite induced transport systems are significantly different from those in normal human cells. Hence, such systems are of considerable interest for their potential use in anti-malarial chemotherapy, both by (i). inhibiting the transport and hence depriving the parasite of nutrients essential for its development, or (ii). by designing cytotoxic drugs which selectively enter the parasite through these induced transporter routes and hence cannot enter normal mammalian cells. Since our discovery that optical isomers of nucleosides (such as L- adenosine or L- thymidine) were selectively transported into malaria infected cells through the induced transporter, L-nucleoside drug "carriers" were actively synthesized as potentially new therapeutic agents. The compounds are dinucleoside phosphate dimers, where each "carrier" (a L-nucleoside) has been conjugated to known anti-malarial agents, such as 5'-fluro-uridine through the 3' and 5'-OH and a phosphate group. A very large series of these drugs have been synthesized with varying conjugations. The dimers are extremely toxic against malaria and experimental evidence has confirmed that they are incapable of entering normal mammalian cells. This review discusses their mechanism of action and potential as new anti-malarial chemotherapy as well as the role played by the membrane transport system of malaria infected cells as a target for malaria chemotherapy.

Animals↗

Long-term stability of circumferential silicone sponge scleral buckling exoplants.

PURPOSE: The historical extrusion/explantation rate of silicone sponge scleral buckle exoplants is 3.5 to 24.4%. This contrasts with the published 0.6 to 1.2% explantation rate of solid silicone elements. Previously reported silicone sponge exoplants studies were noncircumferential (quadrantic or multiple). This study was undertaken to assess the long-term stability of 360 degrees circumferentially placed 3 x 5 mm silicone sponge exoplants. METHODS: Interventional case series of 840 consecutive circumferentially placed 3 x 5 mm silicone sponge exoplants. A retrospective review of operative reports and patient charts was performed. RESULTS: A total of 552 patients had documented follow-up over 1 year. Median follow-up was 32.8 months. Six patients underwent removal of the scleral buckling element (two for diplopia, one acute postoperative infection, and three for extrusion). Median time to removal was 7.3 months. Extenuating circumstances contributed to two of the three extrusions. Of the entire series, fewer than 1% of patients required removal of the silicone sponge implant. Excluding patients with less than 1 year of documented follow-up, the long-term infection/extrusion rate was 0.7%. CONCLUSIONS: Circumferentially placed silicone scleral buckling sponge elements are very stable and are well tolerated. The explantation/extrusion rate is comparable to published solid silicone element series.

Device Removal↗