Valorisation of biowaste digestate through solid state fermentation to produce biopesticides from Bacillus thuringiensis.

The main goal of this work is the production of a biopesticide through solid-state fermentation of biowaste digestate inoculated with Bacillus thuringiensis (Bt) at pilot scale using different configurations of reactors. Fermentations were carried out using insulated and non-insulated, stirred and non-stirred reactors at different scales (10, 22 and 100 L) in order to assess the influence of the reactor configuration on the biopesticide production process. A maximum temperature of 60 °C was reached in 10-L insulated non-stirred reactors where increments of Bt viable cells and spores with respect to initial values of 1.9 and 171.6 respectively, were attained. In contrast, when temperature was regulated by using 22-L non-insulated stirred reactors the increment of viable cells and spores were 0.8 and 1.9, respectively, at a stable temperature of 27 °C. When the non-insulated stirred reactor was scaled up to 100-L, the increase of viable cells and spore counts were 1.2 and 3.8 respectively, with an average temperature of 28 °C. These results demonstrated that the election of a proper reactor configuration is important when considering the development of a new SSF process, especially when dealing with non-conventional substrates as digestate.

Biological and Cognitive Markers of Presenilin1 E280A Autosomal Dominant Alzheimer's Disease: A Comprehensive Review of the Colombian Kindred.

The study of individuals with autosomal dominant Alzheimer's disease affords one of the best opportunities to characterize the biological and cognitive changes of Alzheimer's disease that occur over the course of the preclinical and symptomatic stages. Unifying the knowledge gained from the past three decades of research in the world's largest single-mutation autosomal dominant Alzheimer's disease kindred - a family in Antioquia, Colombia with the E280A mutation in the Presenilin1 gene - will provide new directions for Alzheimer's research and a framework for generalizing the findings from this cohort to the more common sporadic form of Alzheimer's disease. As this specific mutation is virtually 100% penetrant for the development of the disease by midlife, we use a previously defined median age of onset for mild cognitive impairment for this cohort to examine the trajectory of the biological and cognitive markers of the disease as a function of the carriers' estimated years to clinical onset. Studies from this cohort suggest that structural and functional brain abnormalities - such as cortical thinning and hyperactivation in memory networks - as well as differences in biofluid and in vivo measurements of Alzheimer's-related pathological proteins distinguish Presenilin1 E280A mutation carriers from non-carriers as early as childhood, or approximately three decades before the median age of onset of clinical symptoms. We conclude our review with discussion on future directions for Alzheimer's disease research, with specific emphasis on ways to design studies that compare the generalizability of research in autosomal dominant Alzheimer's disease to the larger sporadic Alzheimer's disease population.

[Response to idebenone and multivitamin therapy in Leber's hereditary optic neuropathy]. / Respuesta a la idebenona asociada a multivitaminoterapia en neuropatía óptica hereditaria de Leber.

OBJECTIVE: To ascertain the efficacy of idebenone and multivitamin treatment in Leber's hereditary optic neuropathy (LHON). METHOD: Two patients diagnosed of unilateral LHON were treated with megadoses of idebenone, vitamin C and riboflavin for one year. They were examined clinically before, during and after treatment. RESULTS: No improvement of visual function was observed. Despite the idebenone treatment, in both cases the second eye became involved. CONCLUSIONS: Despite previous reports of visual recovery with idebenone in patients with LHON, our experience shows that an effective treatment for Leber's disease remains to be found.

Long-term depression of excitatory synaptic transmission and its relationship to long-term potentiation.

In many brain areas, including the cerebellar cortex, neocortex, hippocampus, striatum and nucleus accumbens, brief activation of an excitatory pathway can produce long-term depression (LTD) of synaptic transmission. In most preparations, induction of LTD has been shown to require a minimum level of postsynaptic depolarization and a rise in the intracellular Ca2+ concentration [Ca2+]i in the postsynaptic neurone. Thus, induction conditions resemble those described for the initiation of associative long-term potentiation (LTP). However, data from structures susceptible to both LTD and LTP suggest that a stronger depolarization and a greater increase in [Ca2+]i are required to induce LTP than to initiate LTD. The source of Ca2+ appears to be less critical for the differential induction of LTP and LTD than the amplitude of the Ca2+ surge, since the activation of voltage- and ligand-gated Ca2+ conductances as well as the release from intracellular stores have all been shown to contribute to both LTD and LTP induction. LTD is induceable even at inactive synapses if [Ca2+]i is raised to the appropriate level by antidromic or heterosynaptic activation, or by raising the extracellular Ca2+ concentration [Ca2+]o. These conditions suggest a rule (called here the ABS rule) for activity-dependent synaptic modifications that differs from the classical Hebb rule and that can account for both homosynaptic LTD and LTP as well as for heterosynaptic competition and associativity.

New frontiers for the perioperative data method for IOL calculation following corneal refractive surgeries.

PURPOSE: To evaluate the efficiency of the perioperative data method for intraocular lens (IOL) calculation after correction of myopia and hyperopia with different techniques, including reoperated cases. METHODS: Thirty-five eyes (26 patients) that developed cataract after corneal refractive procedures were evaluated retrospectively. They were categorized according to initial error of refraction into myopes and hyperopes and according to types of refractive procedures into ablative, incisional, both, or others. Reoperated cases were also considered. Number of refractive procedures was noted. Time interval between the first procedure and cataract extraction was indicated. Perioperative method was used to calculate the K value. SRK/T formula was used to calculate IOL power. Difference between intended and finally achieved manifest refraction was an indicator for efficiency of the calculation. RESULTS: Postoperatively, 77.2% of cases had manifest refraction +/-1.5 D of intended refraction. There was no difference between myopes and hyperopes in terms of final manifest refraction, best-corrected visual acuity, and difference between intended and finally achieved manifest refraction. Similarly were groups of different types of surgeries. Efficiency of the method decreased with high axial lengths and low IOL powers. Neither the number of refractive surgeries nor time interval between surgeries affected efficiency of the method. CONCLUSIONS: The perioperative data method is equally effective for myopes and hyperopes. The types, numbers of refractive procedures, as well as the time interval between refractive surgery and cataract extraction do not alter the credibility of the method. In high degrees of myopia, the method gives less accurate results.

Synaptic activity modulates the induction of bidirectional synaptic changes in adult mouse hippocampus.

Activity-dependent synaptic plasticity is critical for learning and memory. Considerable attention has been paid to mechanisms that increase or decrease synaptic efficacy, referred to as long-term potentiation (LTP) and long-term depression (LTD), respectively. It is becoming apparent that synaptic activity also modulates the ability to elicit subsequent synaptic changes. We provide direct experimental evidence that this modulation is attributable, at least in part, to variations in the level of postsynaptic depolarization required for inducing plasticity. In slices from adult hippocampal CA1, a brief pairing protocol known to produce LTP can also induce LTD. The voltage-response function for the induction of LTD and LTP in naive synapses exhibits three parts: at a postsynaptic membrane potential during pairing (V(m)) -20 mV, LTP is generated. This function varies with initial synaptic efficacy. In depressed synapses, Theta(-), the V(m) above which LTD is generated, is shifted toward more depolarized V(ms) and Theta(+), the LTD-LTP crossover point or, equivalently, the V(m) above which LTP is induced, toward more polarized V(ms). Conversely in potentiated synapses, Theta(-) is shifted toward more polarized V(ms). Therefore synaptic activity changes synaptic efficacy and accordingly adjusts the voltages for eliciting subsequent synaptic modifications. The concomitant shifts in the voltages for inducing LTD and LTP in opposite directions promote synaptic potentiation and inhibit synaptic depression in depressed synapses and vice versa in potentiated synapses.

The Involvement of N-Methyl-D-Aspartate Receptors in Induction and Maintenance of Long-Term Potentiation in Rat Visual Cortex.

Pyramidal neurons from layers II and III of rat visual cortex slices were studied with intracellular recordings. The involvement of N-methyl-D-aspartate (NMDA) receptors was investigated: (1) in the synaptic response to white matter stimulation; (2) in the induction of long-term potentiation (LTP); and (3) in the maintenance of LTP. Bath application of 25 microM of 2-amino-5-phosphonovalerate (APV), an NMDA receptor antagonist, caused a slight (< 10%) reduction of the amplitude of the synaptic response elicited by white matter stimulation. The APV-sensitive excitatory postsynaptic potential (EPSP) had a longer peak latency and duration than the APV-resistant EPSP. Bath application of 10 microM of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a non-NMDA glutamate receptor antagonist, revealed a CNQX-resistant EPSP in response to white matter stimulation which was APV-sensitive. The time course of the CNQX-resistant EPSP was similar to that of the APV-sensitive EPSP and its onset latency was similar to that of the synaptic response in normal medium. Bath application of the GABA-A antagonist bicuculline (0.1 to 0.5 microM) led to a progressive enhancement of the amplitude of the APV-sensitive EPSP. At bicuculline concentrations above 0.3 microM the amplitude of this EPSP increased with membrane depolarization as was the case for the CNQX-resistant EPSP implying that the NMDA receptors were located on the recorded neuron. The susceptibility of the cells to undergo LTP was tested at various concentrations of bicuculline. The effectiveness of bicuculline treatment was quantified by comparing the amplitudes of the synaptic response to just subthreshold stimuli at two post-stimulus delays: (i) at 22 ms, which corresponds to the time to peak of both the initial inhibitory postsynaptic potential and the APV-sensitive EPSP; and (ii) at 8 - 11 ms post-stimulus, which corresponds to the peak of the postsynaptic potential (PSP) in normal medium. Bath application of APV, 20 min after the conditioning tetanus, allowed the authors to measure the amplitude of the APV-sensitive EPSP in the potentiated response. In normal medium, the ratio of the late over the early PSP amplitude was 33.6 +/- 4.1% and tetanic stimulation failed to induce LTP. The conditions remained the same at bicuculline concentrations of 0.1 to 0.2 microM. At higher concentrations of bicuculline the amplitude ratio of late versus early PSP increased and tetanic stimulation induced LTP. In cells, in which bicuculline had caused small ratio increases, only the APV-sensitive EPSP underwent LTP. In cells in which bicuculline had caused large ratio changes, both the APV-resistant and the APV-sensitive EPSP showed LTP. Together with the previous finding that blockade of NMDA receptors prevents LTP (Artola and Singer, 1987) these results suggest that there is a threshold for LTP induction, which is only reached if NMDA receptor-gated channels are sufficiently activated. The data indicate further that the NMDA receptor-mediated EPSP is itself susceptible to LTP whereby its LTP threshold is lower than that of the APV-resistant EPSP. Given the different LTP thresholds of the APV-resistant and APV-sensitive EPSPs, the possibility is raised that their potentiation depends on different mechanisms.

Enkephalins are associated with adrenergic granules in bovine adrenal medulla.

The subcellular localization of enkephalins was studied in the bovine adrenal medulla. In the adrenal medulla enkephalins (Met-enkephalin, Leu-enkephalin, Met-enkephalin-Arg6-Phe7 and Met-enkephalin-Arg6-Gly7-Leu8) are found free and in the form of cryptic peptides included in larger precursors. Total Met-enkephalin immunoreactivity, which includes free and cryptic peptides, was determined after a sequential enzymatic treatment with trypsin and carboxypeptidase B. Total Met-enkephalin immunoreactivity, dopamine beta-hydroxylase and catecholamines were found to have a parallel distribution in the various subcellular fractions. The bulk of the total Met-enkephalin immunoreactivity (42%) was recovered in the large granule fraction. The large granule fraction also contained 38% of the total dopamine beta-hydroxylase activity, and 42% of the total catecholamines. Enkephalins are thus concentrated in the chromaffin granules. Chromaffin granules were also separated according to the method of Terland & coworkers into two fractions: one containing the dense noradrenergic vesicles and the other containing lighter adrenergic vesicles. Total Met-enkephalin immunoreactivity was restricted to the fractions containing the lighter adrenergic vesicles. In these fractions the molar ratio of adrenaline to total Met-enkephalin immunoreactivity was 97. This study is in accord with immunocytochemical observations which have indicated that enkephalins are located in adrenergic and not in the noradrenergic cells in the bovine adrenal medulla.

Increased spike broadening and slow afterhyperpolarization in CA1 pyramidal cells of streptozotocin-induced diabetic rats.

Diabetes mellitus is associated with impairments of cognitive function both in humans and animal models. In diabetic rats cognitive deficits are related to alterations in activity-dependent synaptic plasticity in the hippocampus. Many similarities with the pathophysiology of normal brain aging have been noted, and the view emerges that the effects of diabetes on the brain are best described as "accelerated brain aging."In the present study we examined whether CA1 pyramidal neurons from streptozotocin-induced diabetic rats display an increased slow afterhyperpolarization, often considered as a hallmark of neuronal aging. We found no differences in resting membrane potential, input resistance, membrane time-constant, and action potential amplitude and duration between CA1 pyramidal neurons from streptozotocin-induced diabetic and age-matched control rats. During a train of action potentials, however, there is an increased broadening of the action potentials in diabetic animals, so-called "spike broadening." The amplitude of the slow afterhyperpolarization elicited by a train of action potentials is indeed increased in diabetic animals. Interestingly, when the slow afterhyperpolarization is elicited by a Ca(2+) spike, there is no difference between control and diabetic rats. This indicates that the increased slow afterhyperpolarization in diabetes is likely to be due to an increased Ca(2+) influx resulting from the increased spike broadening. These data underscore the notion that the diabetic brain at the neuronal level shares properties with brain aging.

Elimination of barium sulphate from acrylic bone cements. Use of two iodine-containing monomers.

The aim of this work is to present a new approach to joint arthroplasty failure related to bone cement mantle. As barium sulphate is considered one of the main causes of mechanical weakness in the cement, we substituted this inorganic radiopacifier of the solid component for radiopaque monomers in the liquid component. We obtained two different cements, one containing 5 vol% 2-[2',3',5'-triiodobenzoyl] ethyl methacrylate (TIBMA) and the other containing 3,5-diiodine salicylic methacrylate (DISMA). In both cases, the mechanical properties of these new cements were better than those of the barium sulphate-containing cement. The radiopacity obtained was comparable to that of the aforementioned cement and all the samples showed good biocompatibility.

Different threshold levels of postsynaptic [Ca2+]i have to be reached to induce LTP and LTD in neocortical pyramidal cells.

Changes in [Ca2+]i were measured in layer II-III pyramid cells of the rat visual cortex slices during application of either LTP or LTD inducing stimulation protocols. At dendritic sites activated by the stimulated afferents [Ca2+]i reached higher amplitudes and decayed more slowly with LTP than with LTD inducing stimuli. In the presence of Ca2+ chelators, the stimulation protocol that would normally produce LTP induced either LTD or failed to induce a synaptic modifications altogether. These results support the hypothesis that the polarity of synaptic gain changes depends on the magnitude of postsynaptic [Ca2+]i responses, the induction of LTP requiring a more pronounced surge of [Ca2+]i than the induction of LTD.

GABA-like activity in in vitro slices of the rat visual cortex: immunocytochemistry and electrophysiology.

Using antisera raised against gamma-aminobutyric acid (GABA), GABA-like immunoreactivity was determined in in vitro slices fixed after various incubation times. Synaptic efficacy of GABAergic innervation was concurrently assessed in adjacent slices by intracellular recordings. We show that GABA-like immunoreactivity dramatically decreases already after one hour of incubation and remains low throughout the following hours. Nevertheless robust GABA-mediated synaptic potentials are recordable for more than 8 h.

Agonists of cholinergic and noradrenergic receptors facilitate synergistically the induction of long-term potentiation in slices of rat visual cortex.

Acetylcholine (ACh) and noradrenaline (NA) have been shown to facilitate experience-dependent modifications of synaptic connectivity during postnatal development of the kitten visual cortex. To further investigate the mechanisms of this facilitation we studied the effects of these neuromodulators in an in vitro model of use-dependent synaptic plasticity. We have chosen long-term potentiation (LTP) in rat visual cortex slices because it shares several features with the in vivo model. In both cases induction of synaptic modifications requires that postsynaptic activation reaches a critical threshold and in both cases changes are induced more easily in young animals and when N-methyl-D-aspartate (NMDA) receptor-gated conductances are activated. Intracellular recordings were obtained from regular spiking cells in supragranular layers of rat visual cortex and LTP was induced by tetanic stimulation of the underlying white matter. Both cholinergic and noradrenergic agonists raised the probability that tetanic stimuli induced LTP and as in vivo they acted synergistically. These effects were mediated by agonists of muscarinic and beta-receptors, respectively. The agonists of both receptor systems enhanced the depolarizing response to the tetanus and increased NMDA receptor-gated conductances during this response. We suggest that this mode of action also accounts for the facilitatory effects which ACh and NA have on use-dependent synaptic plasticity in the developing visual cortex.

Developmental changes in the susceptibility to long-term potentiation of neurones in rat visual cortex slices.

We investigated with intracellular recordings from rat visual cortex slices whether the susceptibility to undergo long-term potentiation (LTP) is age-dependent and whether it is correlated with the expression of synaptic responses mediated by N-methyl-D-aspartate (NMDA) receptors. Test and tetanic stimuli were applied to the white matter and post-tetanic modifications of the amplitude of postsynaptic potentials (PSPs) were assessed in regular spiking cells of supragranular layers. At 2 weeks of age, the amplitudes of early (8-10 ms post-stimulus) and late (20 ms post-stimulus) PSP-components increased after tetanic stimulation to 137.1 +/- 13.4% and 141.3 +/- 12.1% of the pretetanic controls, respectively. At 3 weeks, potentiation of both PSP-components was less pronounced but still significant, the late component being on average more potentiated than the early one. At 4 weeks, PSPs were no longer potentiated. Bath application of 25 microM DL-2-amino-5-phosphonovalerate (APV), an NMDA receptor antagonist, blocked LTP induction both at 2 and at 3 weeks. We also studied developmental changes of two synaptic responses known to influence the susceptibility of cortical neurones to LTP, the NMDA receptor-mediated excitatory PSP (EPSP) and the initial inhibitory PSP (iIPSP). The amplitude of the APV-sensitive EPSP decreased with age and reached adult values in 4-week-old animals. The iIPSPs were pronounced already at 2 weeks and showed no marked change during further development. The results suggest a close correlation between the susceptibility to undergo LTP and the extent to which NMDA receptor-gated conductances contribute to the synaptic response.(ABSTRACT TRUNCATED AT 250 WORDS)

Retinal detachment as a potential hazard in surgical correction of severe myopia with phakic anterior chamber lenses.

Phakic anterior chamber lenses have been proposed as an effective refractive surgical procedure for the correction of severe myopias. We managed three cases of retinal detachment that complicated this operation. Two patients had retinal detachment in the immediate postoperative period at the fourth and sixth weeks, respectively. Both patients had preoperative equatorial lattice degeneration, which was prophylactically managed with argon laser in one case. The third patient developed retinal detachment at the eighth postoperative month and was associated with a severe fibrinoid uveitis and a combined exudative and rhegmatogenous retinal detachment. This third patient did not have any previous retinal degenerative lesion. Scleral buckling was successful in two of the patients, whereas the patient with preoperative inflammation required vitreous surgery because of proliferative vitreoretinopathy. The retinas were reattached in all three patients without explanting the phakic anterior chamber lens, but severe loss of visual acuity occurred in one patient. Retinal detachment should be regarded as a potentially important hazard in this type of refractive surgery.

Laser in situ keratomileusis for treatment of residual myopia after photorefractive keratectomy.

PURPOSE: To evaluate the results of laser in situ keratomileusis after photorefractive keratectomy. METHODS: Eighty eyes of 80 patients with residual myopia after photorefractive keratectomy were reoperated with laser in situ keratomileusis. The study was retrospective. Laser in situ keratomileusis was performed using the automated corneal shaper microkeratome and Chiron Technolas 217-C d1 excimer laser. Data measured after laser in situ keratomileusis included uncorrected visual acuity, best-corrected visual acuity, refraction, haze, pachymetry, and keratometry. The follow-up was at least 12 +/- 1.6 months (range, 12 to 15 months). RESULTS: After laser in situ keratomileusis the mean spherical equivalent was -0.24 diopters +/- 0.78. (range, -3 to +1.5) at 12 months, and the mean uncorrected visual acuity was 0.76 diopters +/- 0.24 (range, 0.1 to 1). Sixty-five eyes (81.3%) had various degrees of haze after laser in situ keratomileusis. One eye (1.2%) lost 2 lines of best-corrected visual acuity. CONCLUSIONS: Laser in situ keratomileusis enhancement may be a good alternative to correct residual myopia and astigmatism after primary photorefractive keratectomy. Corneal haze is a common problem in these eyes, and the treatment after laser in situ keratomileusis enhancement should be the same as the treatment after primary photorefractive keratectomy.

Correction of hyperopia induced by photorefractive keratectomy using non-contact Ho:YAG laser thermal keratoplasty.

PURPOSE: To evaluate the safety and effectiveness of non-contact holmium:YAG laser thermal keratoplasty in correcting hyperopia induced by photorefractive keratectomy (PRK). METHODS: Non-contact holmium:YAG laser thermal keratoplasty was applied to 14 eyes with significant hyperopia induced by PRK. The mean spherical equivalent refraction before holmium:YAG laser thermal keratoplasty was +4.20 +/- 1.80 diopters (D) (range, +1.75 to +6.25 D). The results were evaluated 12 months after holmium:YAG laser thermal keratoplasty. RESULTS: No sight-threatening complications occurred. Recovery of spectacle-corrected visual acuity took from 2 to 6 weeks. The immediate significant myopic shift that developed in all eyes gradually receded over 6 to 8 weeks. All eyes were relatively stable after 9 months. At 12 months, there was no statistically significant difference (p < .005) between the mean preoperative spectacle-corrected visual acuity (0.71 +/- 0.12) and the mean postoperative uncorrected visual acuity (0.65 +/- 0.28). At 12 months there was a mean increase of 4.60 +/- 1.20 D in central keratometric power. Total regression did not occur in any eye. CONCLUSIONS: Non-contact holmium:YAG laser thermal keratoplasty offers a safe and effective alternative to correct PRK-induced hyperopia.

Laser in situ keratomileusis to correct residual myopia after cataract surgery.

PURPOSE: To evaluate the effectiveness, predictability, and safety of laser in situ keratomileusis (LASIK) for correcting residual myopia after cataract surgery with intraocular lens implantation. METHODS: Twenty-two eyes of 22 patients underwent LASIK for the correction of residual myopia after cataract surgery. LASIK was carried out using the Chiron Automated Corneal Shaper and the NIDEK EC-5000 excimer laser. In all eyes, the follow-up was 12 months. RESULTS: Before LASIK, 1 eye (4.5%) had an uncorrected visual acuity of 0.5 or better; 12 months after LASIK, 10 eyes (45.4%) achieved this level of visual acuity and 0 eyes achieved 1.00 or better. Before LASIK, mean refraction was -2.90 +/- 1.80 D; 12 months after LASIK it decreased significantly to 0.40 +/- 0.60 D (P < .01). In 18 eyes (81.8%) at 12 months after LASIK, spherical equivalent refraction was within +/-1.00 D of emmetropia; 11 eyes (50%) were within 0.50 D. No vision-threatening complications occurred. CONCLUSION: LASIK with the Automated Corneal Shaper and Nidek EC-5000 excimer laser was an effective, predictable, stable, and safe procedure for correcting residual myopia after cataract surgery. No intraocular lens or cataract incision related complications occurred when LASIK was performed at least 3 months after phacoemulsification.

Correcting simple myopic astigmatism with the excimer laser.

For one year we followed 46 eyes that had photoastigmatic refractive keratectomy with an excimer laser to correct simple myopic astigmatism. Mean preoperative cylinder was -2.50 +/- 0.70 diopters (D); mean preoperative best corrected visual acuity was 20/25 +/- 1 Snellen line. Mean postoperative refraction one year after surgery was -0.5 +/- 0.2, and mean uncorrected visual acuity was 20/25 +/- 1 Snellen line. In all eyes, the final axis of the residual cylinder was +/- 5 degrees around the preoperative axis. Uncorrected visual acuity equaled best preoperative acuity in 24 eyes. Eight eyes gained one line of best corrected visual acuity, six gained more than one line, and eight lost one line. No patient lost more than one line of uncorrected visual acuity. No significant complications such as haze, halos, eccentric ablation, or hypercorrection were observed.

Retinal detachment in myopic eyes after photorefractive keratectomy.

PURPOSE: To analyze the incidence and characteristics of retinal detachment (RD) in myopic patients who had photorefractive keratectomy (PRK). SETTING: Universidad Miguel Hernández, Instituto Oftalmológico de Alicante, Alicante, Spain. METHODS: The incidence of RD in 5936 consecutive eyes that had PRK to correct myopia was studied. Mean follow-up was 38.5 months +/- 17.4 (SD). RESULTS: Retinal detachment occurred in 5 eyes (0.08%); 2 in women and 3 in men. The mean interval between PRK and RD was 21. 00 +/- 15.89 months (range 9 to 48 months). The mean best corrected visual acuity (BCVA) after PRK and before RD development was 20/81 (range 20/200 to 20/25). After RD repair, the mean BCVA was 20/460 (range 20/2000 to 20/29). In 4 of the 5 eyes, BCVA after RD was within 1 line of the preoperative value; in 1 eye, it decreased from 20/40 to 20/2000. The mean spherical equivalent (SE) before RD treatment was -1.35 +/- 1.08 diopters (D) (range 0 to -3.00 D) and after RD treatment, -2.95 +/- 0.83 D (range -2.00 to -4.00 D). Differences between SE before and after RD treatment were statistically significant (P =.01, paired Student t test). CONCLUSIONS: The incidence of RD after PRK to correct myopia was 0.08%. In 4 of 5 eyes, there was little or no visual loss; but in the group as a whole, there was a significant increase in myopic SE.