Arvydas Gelzinis

Dynamic visual cryptography (DVC) can be formulated as a discrete-time reconstruction problem for time-averaged moiré fringes generated by oscillatory transformations of periodic gratings. When implemented on digital display hardware, the continuous oscillatory motion must be realized through discrete frames, which may prevent correct reconstruction of higher-order time-averaged fringes due to refresh-rate limitations. In this work, mathematical criteria are derived to ensure the reliable reconstruction of higher-order time-averaged moiré fringes under finite refresh rate constraints. Harmonic, stochastic, and rectangular temporal waveforms are examined within a unified framework based on the number of frames per oscillation period and the discrete structure of the resulting time-averaged intensity distribution. Stochastic waveforms are shown to not guaranty reproducible fringe formation. For harmonic modulation with a 240 Hz display refresh rate and a 50 Hz oscillation frequency, only four full frames per period are obtained, which is insufficient to reconstruct the third time-averaged moiré fringe requiring at least sixteen frames per period. Rectangular waveforms satisfy the derived reconstruction conditions when the pitch of the grating, the oscillation amplitude, and the resolution of the rendered grating meet explicit constraints. These results establish quantitative parameter bounds for a mathematically consistent software-based DVC implementation on digital displays.

Background: Leber’s hereditary optic neuropathy (LHON) is the most common mitochondrial disorder and an inherited optic neuropathy. Recently, two different LHON inheritance types have been discovered: mitochondrially inherited LHON (mtLHON) and autosomal recessive LHON (arLHON). Our case report is the first diagnosed case of arLHON in a patient of Lithuanian descent and confirms the DnaJ Heat Shock Protein Family (Hsp40) Member C30 (DNAJC30) c.152A>G p.(Tyr51Cys) founder variant. Case Presentation: A 34-year-old Lithuanian man complained of headache and sudden, painless loss of central vision in his right eye. On examination, the visual acuity of the right and left eyes was 0.1 and 1.0, respectively. Visual-field examination revealed a central scotoma in the right eye, and visual evoked potentials (VEPs) showed prolonged latency in both eyes. Optical coherence tomography showed thickening of the retinal nerve fiber layer in the upper quadrant of the optic disk in the left eye. Magnetic resonance imaging of the head showed evidence of optic nerve inflammation in the right eye. Blood tests were within normal range and showed no signs of inflammation. Retrobulbar neuritis of the right eye was suspected, and the patient was treated with steroids, which did not improve visual acuity. He later developed visual loss in the left eye as well. A genetic origin of the optic neuropathy was suspected, and a complete mitochondrial DNA analysis was performed, but it did not reveal any pathologic mutations. Over time, the visual acuity of both eyes slowly deteriorated, and the retinal nerve fiber layer (RNFL) thinning of the optic disks progressed. A multidisciplinary team of specialists concluded that vasculitis or infectious disease was unlikely to be the cause of the vision loss, and a genetic cause for the disease was still suspected, although a first-stage genetic test did not yield the diagnosis. Thirty-three months after disease onset, whole-exome sequencing revealed a pathogenic variant in the DNAJC30 gene, leading to the diagnosis of arLHON. Treatment with Idebenone was started 35 months after the onset of the disease, resulting in no significant worsening of the patient’s condition. Conclusion: This case highlights the importance of considering arLHON as a possible diagnosis for patients with optic neuropathy, because the phenotype of arLHON appears to be identical to that of mtLHON and cannot be distinguished by clinicians.

Background and Objectives: Myopia is the most widespread ocular disorder globally and its prevalence has been increasing over the past decades. Atropine eye drops stand out as the only pharmacological intervention used in clinical practice to control myopia progression. The aim of this study was to explore the effect of 0.01% atropine eye drops on myopia progression. Patients and Methods: Healthy children aged 6–12 years with cycloplegic spherical equivalent (SE) from −0.5 D to −5.0 D and astigmatism ≤1.5 D were included. Myopia progression was assessed by changes in SE and axial length (AL) over 1 year and SE changes 1 year before the study enrollment and during the 1-year follow-up. Adverse events were evaluated based on complaints reported by either parents or the children themselves during follow-up visits. Results: The analysis involved 55 patients in the 0.01% atropine eye drops group and 66 in the control group. After the 1-year follow-up, the change in SE was −0.50 (−2.25–0.50) D in the control group compared to −0.50 (−1.50–0.50) D in the 0.01% atropine group (p = 0.935); AL change was 0.31 (0.18) mm in the control group and 0.29 (0.18) mm in the 0.01% atropine group (p = 0.480). The change in SE was −0.68 (−2.0–−0.25) D/year before the study and remained similar −0.50 (−2.25–0.25) D over the 1-year follow-up in the control group (p = 0.111); SE change was reduced from −1.01 (−2.0–−0.25) D/year before the study to −0.50 (−1.5–0.5) D over the 1-year follow-up in the 0.01% atropine group (p < 0.001). In the 0.01% atropine group, ten (16.4%) children experienced mild adverse events, including blurred near vision, ocular discomfort, photophobia, dry eyes, and anisocoria. Conclusions: Compared to the control group, the administration of 0.01% atropine eye drops demonstrated no significant effect on changes in SE and AL over a 1-year follow-up. However, children in the 0.01% atropine group initially experienced higher myopia progression, which decreased with treatment over the course of 1 year. Future studies should explore the long-term effects, rebound effects, potential genetic associations, and efficacy of higher doses of atropine in managing myopia progression.

Objective: To investigate the efficacy and safety of one-year treatment with 0.03% atropine eye drops for slowing myopia progression among children aged 6–12 years. Methods: Healthy Caucasian children aged 6–12 years with cycloplegic spherical equivalent (SE) from −1.0 D to −5.0 D and astigmatism and anisometropia ≤1.5 D were included. Changes in mean axial length (AL) and objective SE as well as changes in intraocular pressure (IOP), central corneal thickness (CCT), anterior chamber depth (ACD) and lens thickness (LT) were assessed in the 0.03% atropine eye drops group and the control group from baseline through the 1-year follow-up. The proportion of participants showing myopia progression of p = 0.024). The change in AL was 0.19 (0.17) mm in the 0.03% atropine group, compared to 0.31 (0.20) mm in the control group (p = 0.015). There were no significant differences in changes of IOP, CCT and LT between the groups (all p ≥ 0.05). The 0.03% atropine group had a significantly greater increase in ACD compared to the control group (p = 0.015). In total, 64.5% of patients in the 0.03% atropine group showed progression p = 0.032). Adverse events were reported in 13 (35.0%) out of 37 patients in the treatment group, leading to discontinuation of the eye drops in six (16.0%) cases. None of the adverse events were severe. Conclusions: Despite a higher incidence of adverse events, 0.03% atropine eye drops effectively slowed the progression of myopia over 1-year.