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[Did the tapir infect the ape of vice versa? A new technique for tracing tuberculosis].
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Great apes and rhesus monkeys as subjects for psychopharmacological studies of stimulants and depressants.
A group of experiments is described in which chimpanzees and orangutans are utilized as subjects in research projects designed to evaluate the effects of stimulant and depressant drugs on learning and performance. Efficiency of performance on a task which measures spaced responding was impaired when subjects smoked cigarettes containing delta9-tetrahydrocannabinol prior to testing. In a sequential learning task, these subjects also demonstrated reduced performance when stimulatn drugs were orally administered before testing. Depressant drugs did not produce comparable decrements in sequential learning performance. Physical and behavioral tolerance and dependence on ethanol were investigated in rhesus monkey subjects using a variety of experimental procedures, including forced oral acceptance, intragastric intubation, intravenous infusion, and conditioned voluntary oral acceptance.
Yes, giants, neither diseased nor apes.
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Nuclear expression of apurinic/apyrimidinic endonuclease increases with progression of ovarian carcinomas.
OBJECTIVE: Apurinic/apyrimidinic endonuclease (APE alias Ref-1) is a key enzyme in the base excision repair pathway. Besides its function in DNA repair, APE serves to maintain several transcription factors in an active reduced state such as c-Fos, c-Jun, NF-kappaB, p53 and HIF-1alpha, all of which have been shown to play a role in tumorigenesis. Because of the importance of APE in maintaining genomic stability and gene regulation, we examined whether APE expression is associated with survival and histopathological parameters of patients with ovarian cancer. METHODS: Tissue sections of primary epithelial ovarian carcinomas from 141 patients were immunostained using a monoclonal antibody directed against APE. RESULTS: Nuclear expression of APE was clearly associated with progression of ovarian carcinomas. Patients with Federation of Gynecology and Obstetrics (FIGO) stages III and IV showed a higher nuclear APE expression level than patients with FIGO stages I and II (P < 0.0001). Similarly, nuclear APE expression was associated with histological grading (grade 1 vs. 2 vs. 3; P = 0.025). In contrast, cytoplasmic and stromal APE expression were not associated with progression. The fraction of APE-positive nuclei (P = 0.0185), the intensity of nuclear staining (P = 0.0496) and a combination of both (P = 0.0070) were associated with survival of ovarian cancer patients, as evidenced by a univariable proportional hazards model. CONCLUSIONS: Multivariable analysis, adjusted to FIGO stage, histological grade and type as well as residual tumor after surgery showed that APE is not independent from "classical" prognostic factors of ovarian cancer. An unexpected observation was the inverse correlation between nuclear and cytoplasmic expression of APE. Tumors with strong cytoplasmic APE reactivity showed a higher fraction of APE-negative nuclei than tumors with weak or negative cytoplasmic APE expression (P = 0.045). This suggests that nuclear translocation of APE is impaired during ovarian carcinogenesis. In conclusion, we have shown that nuclear APE expression increases during tumor progression. This suggests that increased base excision repair capacity and/or APE-mediated activation of transcription factors may contribute to more aggressive proliferation of ovarian carcinomas.
Isolation and characterisation of five neurotoxic and cardiotoxic polypeptides from the sea anemone Anthopleura elegantissima.
Five toxins (APE 1 to APE 5) of the sea anemone species Anthopleura elegantissima (Brandt) have been isolated from a toxic by-product fraction of its concentrated crude watery-methanolic extract, prepared previously for the isolation of a neuropeptide (the head-activator) by Schaller and Bodenmüller (Proc. Natl. Acad. Sci. USA 78 (1981) 7000) from 200kg sea anemones. Toxin purification was performed by desalting of the starting material by dialysis (MWCO 3500) against distilled water, anion exchange chromatography on QAE-Sephadex A25 at pH 8, twice gel filtration on Sephadex G50 m, repeated chromatography on QAE-Sephadex at pH 10 and chromatography on the cation exchanger Fractogel EMD SO(3)(-)-650 M.Final purification of the toxins was achieved by HPLC on MN SP 250/10 Nucleosil 500-5 C(18) PPN and MN SP 250/21 Nucleosil 300-7 C(18). Each toxin was composed of at least two isotoxins of which APE 1-1, APE 1-2, APE 2-1, APE 2-2 and APE 5-3 were isolated in preparative scale. With exception of APE 5-3 the sequences of the isotoxins have been elucidated. They resemble the 47 residue type-I long polypeptide toxins native to Anemonia sulcata (Pennant). All isotoxins paralyse the shore crab (Carcinus maenas) by tetanic contractions after i.m. application. The toxins modify current passing through the fast Na(+) channel in neuroblastoma cells, leading to delayed and incomplete inactivation. APE 1-1, APE 2-1 and APE 5-3 produce a positive inotropic effect in mammalian heart muscle, although they differ in potency. The order of potency is APE 2-1>APE 1-1>APE 5-3 (i.e. threshold concentrations are 1, 10 and 300nM, respectively). In addition, they enhance the spontaneous beating frequency in isolated right atria (guinea pig). The most potent cardiotoxic isotoxin is APE 2-1, its sequence is identical with that of AP-C, a toxin isolated and characterised previously by Norton et al. (Drugs and Foods from the Sea, 1978, University of Oklahoma Press, p. 37-50).LD50 APE 2-1:1 micro g/kg b.w. C. maenas (i.m.). LD50 APE 1-1:10 microg/kg b.w. C. maenas (i. m.). LD50 APE 5-3:50 microg/kg b.w. C. maenas (i.m.).
N-(2-hydroxypropyl)methacrylamide copolymer-6-(3-aminopropyl)-ellipticine conjugates. Synthesis, in vitro, and preliminary in vivo evaluation.
Ellipticine derivatives have potential as anticancer drugs. Their clinical use has been limited, however, by poor solubility and host toxicity. As N-(2-hydroxypropyl)methacrylamide (HPMA) copolymer-anticancer conjugates are showing promise in early clinical trials, a series of novel HPMA copolymer conjugates have been prepared containing the 6-(3-aminopropyl)-ellipticine derivative (APE, NSC176328). Drug was linked to the polymer via GFLG or GG peptide side chains. To optimize biological behavior, HPMA copolymer-GFLG-APE conjugates with different drug loading (total APE: 2.3-7% w/w; free APE: <0.1% w/w) were synthesized. Conjugation of APE to HPMA copolymers considerably increased its aqueous solubility (>10-fold). HPMA copolymer-GG-APE did not liberate drug in the presence of isolated lysosomal enzymes (tritosomes), but HPMA copolymer-GFLG-APE released APE to a maximum of 60% after 5 h. The rate of drug release was influenced by drug loading; lower loading led to greater release. Whereas free APE (35 microg/mL) caused significant hemolysis (50% after 1 h), HPMA copolymer-APE conjugates were not hemolytic up to 300 microg/mL (APE-equiv). As would be expected from its cellular pharmacokinetics, HPMA copolymer-GFLG-APE was >75 times less cytotoxic than free drug (IC(50) approximately 0.4 microg/mL) against B16F10 melanoma in vitro. However, in vivo when tested in mice bearing s.c. B16F10 melanoma, HPMA copolymer-GFLG-APE (1-10 mg/kg single dose, APE-equiv) given i.p. was somewhat more active (highest T/C value of 143%) than free APE (1 mg/kg) (T/C =127%). HPMA copolymer-APE conjugates warrant further evaluation as potential anticancer agents.
Activation of muscarinic K+ channels by arecaidine propargyl ester in isolated guinea-pig atrial myocytes.
Arecaidine propargyl ester (APE) was developed as a potential candidate compound for the treatment of Alzheimer's disease. APE has been shown to have cardiovascular effects. APE produces negative chronotropic and inotropic effects in isolated atria. However, the ionic mechanisms underlying the cardiovascular effects of APE in guinea-pig atria are unclear. The aims of this study were: (1) to examine the shortening effect of APE on action potential duration (APD) and to compare the difference in potency between APE and muscarine in isolated single guinea-pig atrial myocytes by using the current clamp method, (2) to examine by using patch clamp techniques the ionic mechanisms underlying the cardiac effects of APE, and (3) to determine whether the cardiac effects caused by APE affect the usefulness of APE as a potential candidate for the treatment of Alzheimer's disease. The APE significantly reduced the APD in guinea-pig atria and produced no direct effect on ventricular myocytes. APE is approximately 20 times as potent as muscarine in shortening the APD. Attenuation of the APD was consistently accompanied by a hyperpolarization of the resting membrane potential in a concentration-dependent manner. The APE activated muscarinic K+ channels and increased potassium conductance in guinea-pig atrial myocytes. In the cell-attached configuration, the APE contained in the pipette increased the channel-opening probability and decreased the closed-state time interval. The proposal that APE can be used as a potential remedy for the treatment of Alzheimer's disease should be taken into consideration the undesirable cardiovascular side effects that APE causes at lower concentrations.
Apurinic endonuclease (Ref-1) is induced in mammalian cells by oxidative stress and involved in clastogenic adaptation.
Apurinic endonuclease (APE; also known as Ref-1 protein) is a key enzyme in base excision repair, cleaving apurinic sites that arise spontaneously because of the activity of DNA glycosylases. To address the question of whether APE can be modulated by genotoxic stress affecting cellular protection, we analyzed the expression of APE in Chinese hamster ovary (CHO) cells after treatment with various genotoxic agents. We show that treatment of CHO cells with hydrogen peroxide (H2O2) or sodium hypochlorite (NaOCl) increases the levels of APE mRNA and protein. APE induction was observed 3-9 h after treatment and was accompanied by an increase in APE activity. We also show that the cloned human APE promoter transfected into CHO cells is stimulated by the oxidants, indicating transcriptional activation of the APE gene. When cells were pretreated with NaOCl, inducing APE, and then challenged with H2O2, the clastogenic effect of the challenge dose was significantly reduced, suggesting clastogenic adaptation due to APE induction. To further prove the involvement of APE in adaptation against induced chromosomal breakage, we transfected human APE cDNA driven by an inducible promoter into CHO cells and observed that transient induction of APE reduced the clastogenic effect of H2O2. Overall, the data demonstrate that the APE gene can be activated by oxidative agents, resulting in a transient increase in APE repair activity, which reduces the clastogenic response of cells to an oxidative agent. The protection of cells from chromosomal aberrations seen after prior exposure to oxidants is attributed to an adaptive response to oxidative stress.
Oxidative stress induces E. coli aryl polyene expression, sensitizing the bacterial stress response and modulating the redox environment of innate immune cells.
UNLABELLED: Aryl polyenes (APEs) are specialized polyunsaturated outer membrane lipids that protect their producers from oxidative stress and contribute to biofilm formation. APEs are produced by an abundant biosynthetic gene cluster (BGC) family conserved across Gram-negative bacterial clades. The APE biosynthesis pathway involves 11 different enzymes and culminates in the attachment of APEs to an anchor molecule in the Gram-negative outer membrane. Unlike most other small molecule BGCs, the APE BGC does not contain a dedicated regulatory gene that controls the production of its metabolically costly compounds. Building from our prior observations of APEs' role in acute oxidative stress protection, we use a uropathogenic Escherichia coli (UPEC) strain to show that APE expression conveys a potential competitive advantage characterized by increased early-stage growth, sensitization of the bacterial oxidative stress response, and dampening of the redox stress of innate immune cells after in vitro infection. Our data indicate that APEs could act as a UPEC fitness factor, and in future work, we aim to study their contribution to overall bacterial pathogenicity and survival, as well as how APEs could facilitate the transition from an oxygen-poor environment, such as the gut, to the oxygen-rich environment of the urinary tract. IMPORTANCE: Bacterial pathogens use various mechanisms to achieve a competitive advantage under harsh conditions, such as during interactions with their host. We studied the function of aryl polyenes (APEs), specialized polyunsaturated fatty acids in the outer membrane, in the context of a uropathogenic E. coli strain. APE expression is induced by an oxidative environment and contributes to early-stage growth and sensitization of the oxidative stress response. Furthermore, APE-expressing E. coli dampen the intracellular oxidative milieu of target host phagocytes. These findings suggest a role for APEs as a fitness factor and create opportunities to study their in vivo function and explore them as a potential drug target.
Helicobacter pylori and H2O2 increase AP endonuclease-1/redox factor-1 expression in human gastric epithelial cells.
BACKGROUND & AIMS: Helicobacter pylori infection causes inflammation, accumulation of reactive oxygen species, and oxidative DNA damage in the gastric mucosa. Apurinic/apyrimidinic endonuclease-1 (APE-1)/redox factor-1 (Ref-1) repairs damaged DNA and reductively activates transcription factors, including activator protein-1. Considering that H. pylori generate reactive oxygen species and that reactive oxygen species modulate APE-1/Ref-1 in other cell types, we examined the effect of H. pylori, oxidative stress, and antioxidants on APE-1/Ref-1 expression in human gastric epithelial cells. METHODS: Human gastric epithelial cell lines or cells isolated from mucosal biopsy samples were stimulated with H. pylori, Campylobacter jejuni, and/or H 2 O 2 in the presence or absence of antioxidants. APE-1/Ref-1 expression was assayed by Western blot or reverse-transcription polymerase chain reaction, and its cellular distribution was determined by using indirect conventional and confocal immunofluorescence. New protein synthesis was detected by [S 35 ]methionine labeling. APE-1/Ref-1 function was assessed by using a luciferase-linked reporter construct containing 3 activator protein 1 binding sites. RESULTS: APE-1/Ref-1 protein and messenger RNA were detected in resting gastric epithelial cells. APE-1/Ref-1 protein expression was increased after stimulation with H 2 O 2 or live cag pathogenicity island-bearing H. pylori, but not cag pathogenicity island-negative H. pylori or C. jejuni. H. pylori - or reactive oxygen species-mediated increases in APE-1/Ref-1 expression involved de novo protein synthesis that was inhibited by antioxidants. H. pylori or H 2 O 2 also induced nuclear accumulation of APE-1/Ref-1, and overexpression of APE-1/Ref-1 increased activator protein 1 binding activity. CONCLUSIONS: The data show that H. pylori or reactive oxygen species enhance APE-1/Ref-1 protein synthesis and nuclear accumulation in human gastric epithelial cells and implicate APE-1/Ref-1 in the modulation of the pathogenesis of H. pylori infection.
Human AP endonuclease suppresses DNA mismatch repair activity leading to microsatellite instability.
The multifunctional mammalian apurinic/apyrimidinic (AP) endonuclease (APE) participates in the repair of AP sites in the cellular DNA as well as participating in the redox regulation of the transcription factor function. The function of APE is considered as the rate-limiting step in DNA base excision repair. Paradoxically, an unbalanced increase in APE protein leads to genetic instability. Therefore, we investigated the mechanisms of genetic instability that are induced by APE. Here, we report that the overexpression of APE protein disrupts the repair of DNA mismatches, which results in microsatellite instability (MSI). We found that expression of APE protein led to the suppression of the repair of DNA mismatches in the normal human fibroblast cells. Western blot analysis revealed that hMSH6 protein was markedly reduced in the APE-expressing cells. Moreover, the addition of purified Mutalpha (MSH2 and MSH6 complex) to the extracts from the APE-expressing cells led to the restoration of mismatch repair (MMR) activity. By performing MMR activity assay and MSI analysis, we found that the co-expression of hMSH6 and APE exhibited the microsatellite stability, whereas the expression of APE alone generated the MSI-high phenotype. The APE-mediated decrease in MMR activity described here demonstrates the presence of a new and highly effective APE-mediated mechanism for MSI.
Antibodies to phosphatidylethanolamine in antiphospholipid syndrome and systemic lupus erythematosus: their correlation with anticardiolipin antibodies and beta 2 glycoprotein-I plasma levels.
The sera patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) were tested, by ELISA, for antibodies to phosphatidylethanolamine (aPE), as well as to cardiolipin (aCL) and compared to healthy blood donors (HBD). Both, SLE and APS patients presented a higher titre of IgM-aPE antibodies than normals, while the IgG and IgA aPE reactivity did not differ. APS patients were characterized by higher IgM-aPE antibody titres than SLE patients. In contrast, the predominant isotype of aCL antibodies in APS patients was IgG. The IgM aPE reactivity was correlated with IgM aCL reactivity, while no correlation was observed between the total IgM values and IgM-aPE binding units of sera tested. Since it was shown that beta 2-glycoprotein-I (beta 2-GPI) contributes to a complex antigen by binding to phospholipids and that this antigen is recognized by antiphospholipid antibodies from autoimmune patients, sera beta 2-GPI levels were measured and correlated to aCL and APE activity. Although APS patients had higher beta 2-GPI levels than SLE patients, no correlation was found between the beta 2-GPI levels and IgG/IgM aCL and IgM-aPE reactivities a finding suggesting that in addition to beta 2-GPI, other cofactors for aPE antibodies may exist. These findings indicate that aPE and aCL antibodies co-exist and that the IgM-isotype is predominant in APS. In addition, the IgA and IgG aPE antibodies appear to occur in low titres in these patients, as well as in normals and may exist as natural autoantibodies. We suggest that the high IgM-aPE antibodies may be viewed as a thymus independent process.
A role for matrix metalloproteinase-9 in the hemodynamic changes following acute pulmonary embolism.
BACKGROUND: Matrix metalloproteinases (MMPs) modulate vascular contractility and may affect acute pulmonary embolism (APE)-induced pulmonary hypertension. We examined the effects of the administration of doxycycline (a MMP inhibitor) following APE in anesthetized dogs. METHODS: Sham operated dogs (N=5) received only saline. APE was induced by intravenous injections of microspheres in amounts to increase mean pulmonary artery pressure (MPAP) by 20 mm Hg, and embolized dogs received saline (Emb group, N=8), or doxycycline (10 mg/kg, i.v.) 5 or 30 min of APE (Emb+Doxy 5 and Emb+Doxy 30 groups, N=9 and 8, respectively). Hemodynamic evaluation was performed at baseline and 5-120 after APE. Gelatin zymography of MMP-2 and MMP-9 from plasma samples was performed. RESULTS: No significant hemodynamic changes were found in Sham animals. Embolization increased MPAP by 218+/-16% and the pulmonary vascular resistance index (PVRI) by 289+/-42% in Emb group (both P<0.05). Doxycyline increased the cardiac index by 24+/-5% and reduced PVRI by 23+/-4% 120 min of APE in Doxy 30+Emb group. In addition, doxycyline reduced MPAP and PVRI 30 min after APE with maximum effects seen 120 min after APE (25+/-4% decrease in MPAP and 33+/-6% decrease in PVRI; both P<0.05) in Doxy+5 group. Plasma pro-MMP-9 and MMP-9 levels increased only in Emb group and MMP-2 remained unaltered. CONCLUSIONS: Our study shows that doxycycline attenuates APE-induced pulmonary hypertension, and indicates that MMP-9 has a role in APE-induced pulmonary hypertension. MMP-9 may be a pharmacological target in APE.
Can cryoglobulins interfere with the measurement of IgM antiphosphatidylethanolamine antibodies by ELISA?
Clinical manifestations of the antiphospholipid antibody syndrome (APS) have been recently related to the presence of phosphatidylethanolamine antibodies (aPE). However, it is well known that some molecules such as cryoglobulins, immunoglobulins that undergo a reversible precipitation at low temperatures, may interfere with biological assays. With this in view, we report the case of a patient with APS who was positive for both IgM aPE and type III cryoglobulinemia. Moreover, we show for this patient a potential implication of aPE in the cryoprecipitate formation. To further analyze the potential association between cryoglobulins and aPE, and also the possible consequences for aPE assay, we selected 55 patients according to positivity for both IgM aPE and cryoglobulinemia. Determination of IgM aPE levels was made before and after removal of cryoprecipitate from the serum. Of the 55 selected patients, 52 (95%) presented no significant difference for IgM aPE levels before and after cryoprecipitation. These results were ascertained whatever the aPE levels and clinical status of the patient. Taken together, our results indicate that cryoprecipitation does not interfere in most cases (95%) with the dosage of IgM aPE. Thus, IgM aPE do not appear to be involved in the formation of the cryoprecipitate.
Protective effects of atorvastatin in rat models of acute pulmonary embolism: involvement of matrix metalloproteinase-9.
OBJECTIVE: Matrix metalloproteinases (MMPs) have been implicated in the pathophysiology of acute pulmonary embolism (APE)-induced pulmonary hypertension. Here, we evaluate the effects of atorvastatin pretreatment on APE-induced pulmonary hypertension, 24-hr mortality rate, and changes in plasma and lung MMP-2 and MMP-9 activities. DESIGN: Controlled animal study. SETTING: University research laboratory. SUBJECTS: Male Wistar rats. INTERVENTIONS: Rats received atorvastatin (30 mg/kg/day orally) or tap water for 2 wks. In study 1, we examined whether atorvastatin affected APE-induced pulmonary hypertension by using a rat isolated lung perfusion model of APE. In study 2, we examined whether atorvastatin affects the survival rate after APE, which was induced by rapid intravenous injection of 14 mg/kg of a suspension of microspheres (or saline) into the tail vein. MEASUREMENTS AND MAIN RESULTS: Plasma nitrite/nitrate concentrations were measured by chemiluminescence. Pretreatment with atorvastatin was associated with 49% higher nitrite/nitrate levels compared with controls (p < .05). In study 1, whereas APE increased mean pulmonary artery pressure (MPAP) by 13.0 +/- 1.6 mm Hg in perfused lungs isolated from rats pretreated with water, pretreatment with atorvastatin attenuated by 27% the increases in MPAP after APE. In study 2, pretreatment with atorvastatin was associated with a significant increase in 24-hr survival rate after APE, which was 48% in embolized rats pretreated with water and 64% in rats pretreated with atorvastatin (p < .05). Gelatin zymography of lung and plasma MMP-2 and MMP-9 was performed. Lungs and plasma from embolized rats showed higher levels of both pro- and activated forms of MMP-9 compared with those from nonembolized animals (all p < .05). However, pretreatment with atorvastatin attenuated by 32% the increases in lung-activated MMP-9 levels after APE (p < .05). CONCLUSIONS: These results suggest that pretreatment with atorvastatin attenuates APE-induced pulmonary hypertension and increases 24-hr survival rate by mechanisms that result in attenuated increases in lung activated MMP-9 after APE.
Disturbed right ventricular ejection pattern as a new Doppler echocardiographic sign of acute pulmonary embolism.
Transthoracic echocardiography (TTE) is frequently performed in patients with suspected acute pulmonary embolism (APE) to search for right ventricular (RV) pressure overload. We prospectively assessed the diagnostic value of a new Doppler echocardiographic sign of APE based on the disturbed RV ejection pattern ("60/60 sign") and compared its diagnostic performances with that of the presence of RV pressure overload, as well as with "McConnell sign" based on RV regional wall motion abnormalities. We assessed 100 consecutive patients with clinical suspicion of APE, including those with previous cardiorespiratory diseases. After TTE, all of the patients underwent reference diagnostic tests for APE. The 60/60 sign required RV acceleration time of <or=60 ms in presence of tricuspid insufficiency pressure gradient <or=60 mm Hg. APE was ultimately confirmed in 67 of 100 patients. In 17 of 67 patients, 60/60 sign correctly suggested APE, whereas 2 false-positive results were noted: in pulmonary fibrosis and in acute respiratory distress syndrome following lung resection. McConnell sign was fully specific but was noted in only 13 of 67 patients. Sensitivity and specificity were 81% and 45% for "RV-pressure overload" signs, 25% and 94% for 60/60 sign, and 19% and 100% for McConnell sign. When combined, the 2 latter signs were 94% specific and 36% sensitive in diagnosing APE. Thus, RV overload at echocardiography is not specific for APE. The 60/60 and McConnell signs are insensitive, but are reliable and helpful in bedside diagnosis of APE when direct visualization of the pulmonary arteries is impossible. Combining these 2 signs may increase the sensitivity without compromising the specificity of echocardiographic diagnosis of APE.
Autologous plasmin enzyme in the surgical management of diabetic retinopathy.
PURPOSE: This is a pilot study to assess the use of autologous plasmin enzyme (APE) as an adjunct to vitreous surgery in eyes with advanced diabetic retinopathy. DESIGN: Prospective noncomparative interventional case series. PARTICIPANTS: Seven patients with advanced diabetic retinopathy selected at random from our practice population. METHODS: Seven eyes were treated with APE as an adjunct to standard vitreous surgery. Six eyes had macular tractional retinal detachments, and one eye had refractory macular edema. Three fellow eyes had standard vitreous surgery performed for macular tractional retinal detachments without APE. All 10 eyes had macular edema and background diabetic retinopathy. MAIN OUTCOME MEASURES: The main outcome measures included induction of a posterior vitreous detachment, retinal reattachment, improvement in visual acuity, and resolution of macular edema. RESULTS: All seven APE-treated eyes achieved spontaneous or easy removal of the posterior hyaloid including one eye that had vitreoschisis over areas of detached retina. All eyes treated with APE had resolution of intraretinal edema. Retinas of all eyes treated with APE were reattached. The three fellow eyes were treated by vitreous surgery without APE. Two of the three fellow eyes had reattached retinas, but none had resolution of intraretinal edema without further focal photocoagulation treatment. Mean visual acuity improvement was 0.7 logarithm of the minimum angle of resolution (LogMAR) units in APE-treated eyes and 0.1 LogMAR units in eyes without APE. The average follow-up period was 14 months. CONCLUSIONS: This pilot study suggests that APE may be beneficial in the surgical management of diabetic retinopathy.