ASYMMETRIC LEAVES1 promotes leaf hyponasty in Arabidopsis by light-mediated auxin signaling.

In plants, balancing growth and environmental responses is crucial for maximizing fitness. Close proximity among plants and canopy shade, which negatively impacts reproduction, elicits morphological adjustments such as hypocotyl growth and leaf hyponasty, mainly through changes in light quality and auxin levels. However, how auxin, synthesized from a shaded leaf blade, distally induces elongation of hypocotyl and petiole cells remains to be elucidated. We demonstrated that ASYMMETRIC LEAVES1 (AS1) promotes leaf hyponasty through the regulation of auxin biosynthesis, polar auxin transport, and auxin signaling genes in Arabidopsis (Arabidopsis thaliana). AS1 overexpression leads to elongation of the abaxial petiole cells with auxin accumulation in the petiole, resulting in hyponastic growth, which is abolished by the application of an auxin transport inhibitor to the leaf blade. In addition, the as1 mutant exhibits reduced hypocotyl growth under shade conditions. We observed that AS1 protein accumulates in the nucleus in response to shade or far-red light. Chromatin immunoprecipitation analysis identified the association of AS1 with the promoters of YUCCA8 (YUC8) and INDOLE-3-ACETIC ACID INDUCIBLE 19 (IAA19). In addition, AS1 forms complexes with PHYTOCHROME INTERACTING FACTORs in the nucleus and synergistically induces YUC8 and IAA19 expression. Our findings suggest that AS1 plays a crucial role in facilitating phenotypic plasticity to the surroundings by connecting light and phytohormone action.

Ptr1 and ZAR1 immune receptors confer overlapping and distinct bacterial pathogen effector specificities.

Some nucleotide-binding and leucine-rich repeat receptors (NLRs) indirectly detect pathogen effectors by monitoring their host targets. In Arabidopsis thaliana, RIN4 is targeted by multiple sequence-unrelated effectors and activates immune responses mediated by RPM1 and RPS2. These effectors trigger cell death in Nicotiana benthamiana, but the corresponding NLRs have yet not been identified. To identify N. benthamiana NLRs (NbNLRs) that recognize Arabidopsis RIN4-targeting effectors, we conducted a rapid reverse genetic screen using an NbNLR VIGS library. We identified that the N. benthamiana homolog of Ptr1 (Pseudomonas tomato race 1) recognizes the Pseudomonas effectors AvrRpt2, AvrRpm1, and AvrB. We demonstrated that recognition of the Xanthomonas effector AvrBsT and the Pseudomonas effector HopZ5 is conferred independently by the N. benthamiana homolog of Ptr1 and ZAR1. Interestingly, the recognition of HopZ5 and AvrBsT is contributed unequally by Ptr1 and ZAR1 in N. benthamiana and Capsicum annuum. In addition, we showed that the RLCK XII family protein JIM2 is required for the NbZAR1-dependent recognition of AvrBsT and HopZ5. The recognition of sequence-unrelated effectors by NbPtr1 and NbZAR1 provides an additional example of convergently evolved effector recognition. Identification of key components involved in Ptr1 and ZAR1-mediated immunity could reveal unique mechanisms of expanded effector recognition.

The Ralstonia pseudosolanacearum effector RipE1 is recognized at the plasma membrane by NbPtr1, the Nicotiana benthamiana homologue of Pseudomonas tomato race 1.

The bacterial wilt disease caused by soilborne bacteria of the Ralstonia solanacearum species complex (RSSC) threatens important crops worldwide. Only a few immune receptors conferring resistance to this devastating disease are known so far. Individual RSSC strains deliver around 70 different type III secretion system effectors into host cells to manipulate the plant physiology. RipE1 is an effector conserved across the RSSC and triggers immune responses in the model solanaceous plant Nicotiana benthamiana. Here, we used multiplexed virus-induced gene silencing of the nucleotide-binding and leucine-rich repeat receptor family to identify the genetic basis of RipE1 recognition. Specific silencing of the N. benthamiana homologue of Solanum lycopersicoides Ptr1 (confers resistance to Pseudomonas syringae pv. tomato race 1) gene (NbPtr1) completely abolished RipE1-induced hypersensitive response and immunity to Ralstonia pseudosolanacearum. The expression of the native NbPtr1 coding sequence was sufficient to restore RipE1 recognition in Nb-ptr1 knockout plants. Interestingly, RipE1 association with the host cell plasma membrane was necessary for NbPtr1-dependent recognition. Furthermore, NbPtr1-dependent recognition of RipE1 natural variants is polymorphic, providing additional evidence for the indirect mode of activation of NbPtr1. Altogether, this work supports NbPtr1 relevance for resistance to bacterial wilt disease in Solanaceae.

Diversified host target families mediate convergently evolved effector recognition across plant species.

Recognition of pathogen effectors is a crucial step for triggering plant immunity. Resistance (R) genes often encode for nucleotide-binding leucine-rich repeat receptors (NLRs), and NLRs detect effectors from pathogens to trigger effector-triggered immunity (ETI). NLR recognition of effectors is observed in diverse forms where NLRs directly interact with effectors or indirectly detect effectors by monitoring host guardees/decoys (HGDs). HGDs undergo different biochemical modifications by diverse effectors and expand the effector recognition spectrum of NLRs, contributing robustness to plant immunity. Interestingly, in many cases of the indirect recognition of effectors, HGD families targeted by effectors are conserved across the plant species while NLRs are not. Notably, a family of diversified HGDs can activate multiple non-orthologous NLRs across plant species. Further investigation on HGDs would reveal the mechanistic basis of how the diversification of HGDs confers novel effector recognition by NLRs.

Two plant NLR proteins confer strain-specific resistance conditioned by an effector from Pseudomonas syringae pv. actinidiae.

Pseudomonas syringae pv. actinidiae (Psa) causes bacterial canker, a devastating disease threatening the Actinidia fruit industry. In a search for non-host resistance genes against Psa, we find that the nucleotide-binding leucine-rich repeat receptor (NLR) protein ZAR1 from both Arabidopsis and Nicotiana benthamiana (Nb) recognizes HopZ5 and triggers cell death. The recognition requires ZED1 in Arabidopsis and JIM2 in Nb plants, which are members of the ZRK pseudokinases and known components of the ZAR1 resistosome. Surprisingly, Arabidopsis ZAR1 and RPM1, another NLR known to recognize HopZ5, confer disease resistance to HopZ5 in a strain-specific manner. Thus, ZAR1, but not RPM1, is solely required for resistance to P. s. maculicola ES4326 (Psm) carrying hopZ5, whereas RPM1 is primarily required for resistance to P. s. tomato DC3000 (Pst) carrying hopZ5. Furthermore, the ZAR1-mediated resistance to Psm hopZ5 in Arabidopsis is insensitive to SOBER1, which encodes a deacetylase known to suppress the RPM1-mediated resistance to Pst hopZ5. In addition, hopZ5 enhances P. syringae virulence in the absence of ZAR1 or RPM1 and that SOBER1 abolishes such virulence function. Together the study suggests that ZAR1 may be used for improving Psa resistance in Actinidia and uncovers previously unknown complexity of effector-triggered immunity and effector-triggered virulence.

Assessment for Macular Thickness after Uncomplicated Phacoemulsification Using Optical Coherence Tomography.

PURPOSE: Macular edema including cystoid macular edema is one of the main causes of unfavorable visual outcomes after cataract surgery. The macular thickness and the occurrence of macular edema after uncomplicated cataract surgery was evaluated using optical coherence tomography (OCT) in this study. METHODS: Macular map images were taken by OCT before surgery and at 1 week, 1 month, and 2 months postsurgery. The subjects were classified into two groups (group 1, patients with no macular edema; group 2, patients with macular edema). Group 2 was defined as increase in central macular thickness (CMT) by 30% compared with that before surgery. The risk factors for macular edema were evaluated. Group 2 was divided into two subgroups: subclinical macular edema (group 2A) and cystoid macular edema (group 2B) and they were assessed in terms of the clinical course of best-corrected visual acuity and CMT. RESULTS: A total of 376 patients were enrolled in this study, of which 36 (9.57%, group 2) showed macular edema measured by OCT after the surgery. Univariate analysis for group 1 and 2 revealed that intracameral injection of epinephrine during phacoemulsification was associated with the development of macular edema. In group 2, five patients (1.33%) developed cystoid macular edema. Statistically significant differences in the clinical course of CMT were observed at 2 months (201.2 ± 23.1, 250.0 ± 29.8, and 371.0 ± 160.3 in group 1, group 2A, and group 2B, respectively; p < 0.001) and 1 month postoperatively (198.5 ± 23.6, 237.8 ± 40.9, and 314.0 ± 104.5 in group 1, group 2A, and group 2B, respectively; p < 0.001). Group 2B required additional treatment and eventually achieved best-corrected visual acuity of >0.2 with CMT in the normal range. CONCLUSIONS: The intracameral injection of epinephrine may cause macular edema after uncomplicated cataract surgery. Examination of CMT using OCT is recommended for the early detection of macular edema.

Lipid layer thickness decrease due to meibomian gland dysfunction leads to tear film instability and reflex tear secretion.

PURPOSE: To determine the clinical effects of ocular surface and Meibomian gland parameters on tear film stability among individuals with Meibomian gland dysfunction (MGD), those with aqueous deficient dry eye (ADDE), individuals with both conditions and normal controls. METHODS: Patients were divided into four groups: normal controls, patients with ADDE, patients with MGD, and patients who fulfilled diagnostic criteria for ADDE and MGD (Mixed Group). Data for ocular symptom score, lid margin abnormality, ocular staining, tear break-up time, meiboscore, and lipid layer thickness (LLT) measured by a Lipiview interferometer, Schirmer test, and MGD severity score were collected. RESULTS: A total of 109 patients (109 eyes) were evaluated. In patients with MGD, LLT was significantly lower than the ADDE patients. However, the Schirmer test value was the highest in the MGD group. The LLT negatively correlated with meiboscore and MGD severity score in the MGD group. Significant correlation between Schirmer test value and meiboscore was definite in the MGD group. CONCLUSIONS: Tear fluid secretion is more increased and lipid layer thickness is more decreased in MGD patients than in ADDE patients. Decreased lipid layer thickness caused by MGD-related tear film instability may stimulate reflex tear secretion. The obstructive MGD is more prevalent than hypersecretary MGD.Key messagesThe tear film stability is affected by Mebomian gland dysfunction (MGD). The measurement of the tear film parameters including lipid layer thickness suggests that the obstructive MGD is more prevalent than hypersecretary MGD and the aqueous layer compensates the decreased lipid layer caused by MGD.

Peripapillary hyperreflective ovoid mass-like structures (PHOMS) in children.

BACKGROUND: To analyse structural characteristics and perifoveal/peripapillary vasculature by OCT in children with peripapillary hyperreflective ovoid mass-like structures (PHOMS) and compare the results with those of normal subjects. METHODS: Forty-five patients (84 eyes) under 18 years old with blurry disc margin were evaluated with spectral domain-OCT and swept course-OCT. Patients were divided into four groups, according to presence of PHOMS and then the size of the existing PHOMS. Eyes with visible optic disc drusen (ODD) were not included. Foveal avascular zone (FAZ) and vessel densities from macula and optic disc area were assessed and potential associations between vessel density and structural parameters, such as peripapillary retinal nerve fibre layer (pRNFL), and macular ganglion cell and inner plexiform layer (mGCIPL) thickness, were analysed. RESULTS: Among 45 patients (eighty-four eyes), coexisting buried ODD were found only in eyes with PHOMS. The scleral canal diameter was significantly smaller in PHOMS positive eyes compared to control eyes. Vessel density measurements from the papillary, peripapillary and optic nerve head (ONH) regions in the large PHOMS group were significantly lower compared to the control group (papillary; P = 0.014, peripapillary; P = 0.001, ONH; P = 0.046). FAZ area and macular vessel densities showed no difference compared to normal eyes in all three PHOMS groups. pRNFL and mGCIPL thickness did not differ among four groups and correlations were also not significant. CONCLUSIONS: Children with PHOMS have smaller scleral canal and can entail buried ODD. Vessel densities of optic disc area in large PHOMS eyes are significantly lower than in normal eyes.

Morphological change of the posterior pole following the horizontal strabismus surgery with swept source optical coherence tomography.

Extraocular muscle movement during strabismus surgery causes changes in eyeball shape. Because extraocular muscle insertion is in front of the equator, it is thought that changes due to strabismus surgery mainly occur in the anterior segment. However, changes in the posterior segment of eye may also occur, which may also result in changes in refractive error after strabismus surgery. Using a 3-dimensional reconstruction technique (en face imaging) of the swept source optical coherence tomography, we determined and quantitatively measured the posterior polar change. The deepest interface between Bruch's membrane and the choroid could be identified as the deepest point of the eyeball (DPE), and the location of the DPE relative to the optic disc and the fovea was measured. After lateral rectus muscle recession, the DPE moved away from the fovea, but after medial rectus muscle recession, the DPE moved toward the fovea. The amount of DPE movement differed by age and preoperative refractive error. Our findings suggest that the positional shift of the rectus muscle in horizontal strabismus surgery causes a structural change in the posterior segment of the eye, and the postoperative refractive changes may be related to this shift.

Compressive Optic Neuropathy with a Concurrent Mutation of Leber's Hereditary Optic Neuropathy: A Case Report.

Leber's hereditary optic neuropathy (LHON) is a mitochondrial genetic disease that leads to acute or subacute, painless, bilateral loss of vision, caused by degeneration of retinal ganglion cells that most affects men in their second or third decade of life. We describe a woman with compressive optic neuropathy with a concurrent LHON-associated mitochondrial mutation. Temporal hemifield defect connected to central scotoma and concurrent abduction limitation are diagnostic clues in identifying chiasmal compression with craniopharyngioma. This case emphasizes an awareness of the possible coexistence of compressive and hereditary optic neuropathy.

Long term change of the optic disc and OCT parameters during myopic shift in children with large cup to disc ratio.

PURPOSE: This observational case series was to determine long term optic disc changes in eyes with large cup to disc ratio (CDR) and compare the changes induced by myopic shift during childhood with normal control eyes. METHODS: Children under 15 years of age who developed myopia with serial optic disc photographs and spectral domain (SD)-optical coherence tomography (OCT) images with a minimal interval of three years were evaluated. Children with average CDR ≥ 0.6 on SD-OCT were classified as having large CDR. The ratios of vertical disc diameter (VDD), horizontal disc diameter (HDD), and maximum peripapillary atrophy (PPA) width (PPW) were measured to quantify morphologic changes of optic discs and SD-OCT parameters, such as peripapillary retinal nerve fiber layer (RNFL) thickness and macular ganglion cell and inner plexiform layer (GCIPL) thickness were measured. RESULTS: Of the 82 eyes (82 patients) analyzed, 42 eyes had large CDR and 40 eyes were normal controls. The mean age and refractive error at initial examination were not different between groups (P = 0.33, P = 0.76, respectively). The changes in HDD/VDD and PPW/VDD ratios during follow-up showed no significant difference among the groups (P = 0.45, P = 0.62, respectively). No statistical significance was found in changes in RNFL and GCIPL thickness between the two groups (P = 0.74, P = 0.79, respectively). CONCLUSIONS: Children with enlarged CDR showed changes in optic disc morphology and RNFL/GCIPL thickness similar to normal children during myopic shift.

Genotypic and phenotypic characteristics of Korean children with childhood-onset Leber's hereditary optic neuropathy.

PURPOSE: We sought to identify the phenotypic and genotypic characteristics of Korean children with genetically confirmed Leber's hereditary optic neuropathy (LHON). METHODS: The medical records of 64 genetically confirmed LHON patients were reviewed. Seventeen patients aged 13 years or younger with optic atrophy with positive mitochondrial DNA (mtDNA) mutations were considered to demonstrate childhood-onset LHON. The non-childhood-onset group included 47 patients with genetically confirmed LHON who experienced disease onset later than 13 years of age. The type of mtDNA mutation, visual acuity (VA), color vision, fundus photography, retinal nerve fiber layer (RNFL) thickness, and visual field were investigated. RESULTS: Sequence analysis of the mitochondrial genome revealed five different kinds of LHON-associated mtDNA mutations among our childhood-onset patients, including m.11778G>A (58.8%), m.3496G>T (11.8%), m.3497C>T (5.9%), m.11696G>A (5.9%), and m.14502T>C (5.9%). The mean final best-corrected VA in the childhood-onset group was better than that in the non-childhood-onset group with the value of logMAR 0.29 (0.09-0.75) vs. 0.55 (0.27-1.29) (expressed as median (interquartile range); p = 0.05). Spontaneous visual recovery was observed in 35.3% of the childhood-onset group but in only 12.8% of the non-childhood-onset group (p = 0.04). Eight patients (47.1%) showed interocular asymmetry of the disease, with two presenting true unilateral involvement of the optic nerve and the other six patients demonstrating unilateral subclinical manifestations with bilateral optic atrophy. CONCLUSION: Involvement of secondary mitochondrial mutations was confirmed in patients with childhood-onset LHON. Characteristic clinical features of childhood-onset LHON included a higher proportion of subacute or insidious onset of symptoms, better VA, higher spontaneous recovery, and asymmetrical ocular involvement.

Interocular difference associated with myopic progression following unilateral lateral rectus recession in early school-aged children.

PURPOSE: To compare refractive changes in operated eyes and fellow unoperated eyes following unilateral lateral rectus recession in early school-aged children. STUDY DESIGN: A retrospective case control study. METHODS: The medical records of children under ten years of age with intermittent exotropia who underwent unilateral lateral recession surgery were reviewed. The operated eyes were reviewed and the fellow unoperated eyes were used as control. The rate of myopic progression was calculated by spherical equivalent (SE) changes per year, and by the rate of refractive growth (RRG) equation. RESULTS: SE showed a myopic shift one week after surgery and in the following months, from -1.43 ± 1.84 diopters (D) at 1 week post operation to -1.57 ± 2.22 D at one year and, finally -2.95 ± 2.97 D at the average 4.62 years following surgery. However, the SE shift was not significantly different from the unoperated eye. The low myopia group (under -3.0 D) showed a significantly higher myopic change in the operated eye until one year post operation (p = 0.022). The average myopic shift ratio was -0.53 ± 0.46 D yearly in the operated eye. CONCLUSIONS: This study presents data of a large series of refractive changes secondary to lateral rectus recession, and of long-term myopia progression in Korean population.

Surgical and sensory outcomes in patients with intermittent exotropia according to preoperative refractive error.

BACKGROUND/OBJECTIVES: To analyze the surgical and sensory outcomes of intermittent exotropia according to refractive errors and the factors associated with surgical success. SUBJECTS/METHODS: A total of 326 children were divided into three groups according to preoperative refractive error; hyperopic eyes with SE ≥+2D (hyperopic group), eyes with SE between -1D and +2D (emmetropic group), and myopic eyes with SE ≤-1D (myopic group). The surgical outcomes and the sensory outcomes measured by near and distant stereoacuity were compared among the three groups. RESULTS: The surgical success rate in hyperopic group was significantly lower compared to myopic group at last follow-up (P = 0.012). Preoperative near stereopsis was not different among three groups, however, the distance stereopsis was significantly deteriorated in the hyperopic group compared to the other two groups (Titmus; P = 0.168, FD2; P < 0.001, DR; P = 0.048). There was postoperative improvement in both near and distant stereopsis in all three groups (Titmus; P = 0.009, FD2; P = 0.021, DR; P = 0.036) and no significant difference was found in the postoperative distant stereopsis among the three groups. CONCLUSIONS: Preoperative refractive error is a prognostic factor of surgical success in patients with intermittent exotropia. Patients with hyperopia achieved less favorable surgical outcome compared to myopic patients. The preoperative distant stereoacuity was decreased in hyperopic patients compared to myopic patients, which eventually improved after surgery and showed no significant difference at postoperative measurements.

Changes in axial length in accommodative esotropia patients with minimal hyperopic correction.

PURPOSE: To compare the changes of spherical equivalent refractive error (SER) and axial length (AL) for three years in hyperopic children with minimal undercorrection according to the presence of accommodative esotropia (AE). METHODS: A total of 67 hyperopic children were enrolled. The patients were divided into 3 groups and matched by initial age upon examination; esotropic eyes with AE (AE group), fellow eyes with AE (FE group), and right eyes without esotropia (HE group). Changes of SER and AL were serially measured every six months for three years and collected data were compared among the groups. RESULTS: All three groups underwent significant myopic shift and AL elongation during the follow-up period. However, the least amount of change was found in the AE group. The AE group (-0.96 ± 1.38D) exhibited significantly less change in SER compared to the HE group (-1.76 ± 1.11D) and the FE group (-1.57 ± 1.33D) (both p<0.001). Meanwhile, smaller changes of AL were noticeable in the AE group (0.62 ± 0.88mm) compared to the other two groups (HE 0.99 ± 0.29mm; p<0.001, FE 0.73 ± 0.65mm; p = 0.04). The SER and AL changes were not significantly different between the HE group and FE group. CONCLUSIONS: Esotropic eyes with AE patients with minimal undercorrection exhibited little negative shift of SER and AL elongation compared to not only hyperopic eyes without AE but also fellow eyes with AE.

Clinical Features in Children with Posterior Polymorphous Corneal Dystrophy.

PURPOSE: To describe clinical features in children diagnosed with posterior polymorphous corneal dystrophy (PPCD) in their first or second decade of life. METHODS: A retrospective study was performed with the medical records of seven unrelated Korean pediatric patients who were diagnosed with PPCD and were followed up for a minimum of 3 years. Thorough ocular examinations were performed, including best-corrected visual acuity, intraocular pressure, refractive and keratometric measurements, slit-lamp biomicroscopy, and specular microscopy at all visits. RESULTS: Slit-lamp examinations revealed vesicular lesions in one patient and horizontally parallel band-like endothelial lesions in six patients. Unilateral corneal involvement was displayed in 4 patients, yielding 10 eyes with deep corneal features characteristic of PPCD. Other corneal, iris, or fundus pathologic findings were not detected in all cases. Among four children who were examined in their visual development (approximately under 8 years of age), two cases demonstrated unilateral amblyopia at initial examination and exhibited improved visual acuity after refractive correction and occlusion therapy. Astigmatism more than 1.5D, which is generally considered amblyogenic, was found in 8 among 10 PPCD-affected eyes. A final visual acuity of more than 20/32 was achieved with appropriate refractive correction in all PPCD-affected eyes. There was a negative correlation between the corneal astigmatism and the mean endothelial cell density (ECD) (r = -0.655, P = .011). Initial specular microscopic examinations revealed reduced ECD (1733.0 ± 543.9 cells/mm) composed of enlarged cells (average cell area, 624.8 ± 182.1 µm/cell) in PPCD-affected eyes, compared with those in PPCD-unaffected eyes from our study subjects (P < .001 and P = .005, respectively). A statistically significant percent loss in ECD from initial to 3 years was noted in the PPCD-affected eyes (P = .03). CONCLUSIONS: The awareness and treatment of refractive error are important, especially in children with early-onset PPCD during the reversible period of amblyopia. Long-term monitoring of corneal endothelium is required in pediatric patients with early-onset PPCD based on a significant endothelial loss over 3 years in PPCD-affected eyes.

Relationship between Age and Retinal Nerve Fiber Layer Thickness in Normal Children.

PURPOSE: To evaluate the effect of age and ocular factors on peripapillary retinal nerve fiber layer (RNFL) thickness in children. METHOD: A total of 198 normal subjects aged <19 years received a comprehensive ophthalmologic examination, including measurement of visual acuity, axial length, and cycloplegic refraction. Fast optical coherence tomography RNFL scans were obtained and average RNFL thickness was adjusted for ocular magnification. One eye of each subject was randomly selected as the study eye. The correlations between age and other ocular variables were examined. RESULTS: Mean subject age was 8.61 ± 3.12 years. Average RNFL thickness and ocular magnification-corrected average RNFL thickness were 107.71 ± 11.83 and 103.03 ± 12.53 µm, respectively. There was no significant correlation between observed RNFL thickness and spherical equivalent of the refractive error (SE), axial length, or age (all P >0.05). Corrected RNFL thickness was positively correlated with age and axial length and negatively correlated with SE (P <0.01). Age was negatively correlated with the percent difference between observed and corrected RNFL thickness (P <0.001). Multivariate linear regression analysis showed that both axial length and age were correlated with corrected RNFL thickness in subjects <15 years old (P <0.05). CONCLUSION: The RNFL thickness is likely to be overestimated in children <15 years old. Additionally, an RNFL thickness increase was observed in children <15 years old. Thus, ocular magnification and RNFL thickness increase should be considered when assessing RNFL thickness in patients <15 years old.

Clinical features of posterior microphthalmos associated with papillomacular fold and high hyperopia.

BACKGROUND: The aim was to evaluate the characteristic clinical features of posterior microphthalmos. METHODS: Medical records of four patients (eight eyes) between the ages of three and 31 years with posterior microphthalmos were reviewed retrospectively. Thorough ocular examinations were performed, including visual acuity, intraocular pressure, ocular alignment, axial length, cycloplegic refraction, slitlamp biomicroscopy of the anterior segment and fundus and spectral-domain optical coherent tomography (SD-OCT). RESULTS: All subjects had presented with high hyperopia (+11.0 to +15.75 D) and retinal papillomacular folds in both eyes. They also had reduced bilateral axial length (15.55-18.61 mm), with foreshortening of the posterior segment and a relatively normal anterior segment. Papillomacular retinal folds involving the inner retinal layers and sparing the outer retinal layers, along with the absence of foveal depression, were confirmed by macular SD-OCT. In three patients, we found esodeviations associated with posterior microphthalmos and one of these required strabismic surgery. Concomitant optic nerve hypoplasia and a newly-developed neurosensory retinal detachment were found in one patient. CONCLUSION: Posterior microphthalmos is a developmental arrest of ocular growth. In addition to high hyperopia and retinal papillomacular folds, various types of esotropia, optic disc hypoplasia and neurosensory retinal detachment may accompany posterior microphthalmos. In particular, children with posterior microphthalmos require early appropriate management of the high refractive error and resultant esotropia.

Calpain and Caspase-12 Expression in Lens Epithelial Cells of Diabetic Cataracts.

PURPOSE: To compare the expression of calpain and caspase-12 in human lens epithelial cells (LECs) of cataract patients with or without diabetic retinopathy (DR). DESIGN: Prospective, comparative case series. METHODS: Patients were divided into 4 groups: patients without diabetes mellitus (DM) (Group 1), patients with DM and without diabetic retinopathy (DR) (Group 2), diabetic patients with nonprolifeative DR (NPDR) (Group 3), and diabetic patients with proliferative DR (PDR) (Group 4). Data on DM duration and glycated hemoglobin (HbA1c) level were collected. The LECs were obtained during cataract surgery and immunohistochemical staining was performed for calpain and caspase-12. The reactivity score of each specimen was determined using confocal microscopy. RESULTS: A total of 40 patients (40 eyes) were evaluated, and each group was composed of 10 patients. The expression of calpain and caspase-12 was highest in Group 4, followed by Group 3, Group 2, and Group 1 (P < .001). The expressions were significantly higher with a longer duration of DM, increased HbA1c level, or advanced DR. CONCLUSIONS: Endoplasmic reticulum stress may be associated with apoptosis of LECs, resulting in cataract formation in diabetic patients.