GYVŪNŲ MOKSLŲ FAKULTETAS (12)

Tyrimo tikslas. Įvertinti optinės koherentinės tomografijos (OKT) ir optinės koherentinės tomografijos angiografijos (OKTA) reikšmę nustatant gyslainės ir tinklainės struktūrinius bei kraujotakos pokyčius ir jų sąsajas su arterine hipertenzija (АН). Metodika. Atlikta literatūros analizė. Informacijos ieškota „PubMed“ duomenų bazėje. Į analizę įtraukti 2016-2025 m. publikuoti tyrimai su suaugusiais pacientais, kai OKT ir (arba) OKTA taikyta vertinant gyslainės ir tinklainės pokyčius sergant АН. Taip pat analizuoti tyrimai, kuriuose kontrolinę grupę sudarė sveiki asmenys, neturintys gyslainės arba tinklainės patologijos. Į analizę įtraukti tik anglų kalba parašyti straipsniai, kurių santraukos ir visas tekstas buvo prieinami. Rezultatai. Literatūros duomenys rodo, kad АН lemia reikšmingus gyslainės ir tinklainės kraujotakos pokyčius. Sergantiesiems АН nustatomas gyslainės plonėjimas ir tinklainės paviršinio bei giliojo kapiliarų sluoksnio retėjimas. OKT ir OKTA leidžia aptikti šiuos pokyčius dar iki klinikinių akių dugno pažeidimų, o pavieniai tyrimai rodo galimybę stebėti kraujotakos pokyčius pradėjus gydymą. Išvados. Gyslainės ir tinklainės pokyčiai gali būti ankstyvas АН sukeltos sisteminės kraujagyslių pažaidos žymuo, o OKT ir OKTA leidžia neinvaziškai įvertinti struktūrinius bei kraujotakos pokyčius ir anksti nustatyti kitų su АН susijusių komplikacijų riziką.

Normal-tension glaucoma (NTG) is a chronic optic neuropathy characterized by progressive retinal ganglion cell (RGC) loss and visual field deterioration despite normal intraocular pressure (IOP). Disease progression may occur even with wellcontrolled IOP, indicating IOP-independent pathogenic mechanisms. Neuroprotection aims to preserve RGC function beyond IOP lowering, but its clinical role remains uncertain. A systematic literature review was conducted using the PubMed database, including studies published between 2021 and 2024. 72 articles were screened, and 16 studies were included in the final analysis after applying predefined inclusion and exclusion criteria. Pathophysiological mechanisms of NTG include glutamate-mediated excitotoxicity via NMDA receptors, mitochondrial dysfunction with NAD⁺ depletion, oxidative stress, neuroinflammation, and vascular dysregulation. Brimonidine has demonstrated RGC preservation and reduced inflammatory activity independent of IOP in experimental models, though clinical data show inconsistent effects on ocular perfusion and structural progression. NMDA antagonists such as memantine failed to show benefit in major glaucoma trials, despite limited structural effects in related optic neuropathies. Nicotinamide (vitamin B3) targets mitochondrial and axonal energy failure and shows early functional signals, but definitive outcomes remain unproven. Other agents like citicoline, coenzyme Q10, and metabolic combinations, report modest functional improvements without consistent long-term structural benefit. Rho-kinase inhibitors demonstrate experimental neuroprotective potential, yet clinical confirmation is lacking. Current evidence suggests that neuroprotective strategies in NTG are biologically plausible but clinically inconclusive. Study heterogeneity, small sample sizes, and variable outcome measures limit comparability and interpretation. In patients with progression despite low IOP, assessment of systemic and vascular factors, such as nocturnal hypotension or sleep apnea, may be clinically relevant. To date, no IOP-independent therapy has been proven to halt NTG progression. IOP reduction remains essential, while neuroprotective agents, including brimonidine, may be considered as adjunctive strategies, although clinical evidence remains limited.

The gut–eye axis is an emerging concept linking intestinal dysbiosis with ocular inflammation, including non-infectious uveitis, through immune, barrier, and metabolite-mediated pathways. Preclinical evidence suggests that alterations in the gut microbiome may influence uveitis onset and activity. Microbiome-targeted therapies represent a novel therapeutic direction. A systematic literature review of studies published between 2021 and 2025 was conducted to evaluate microbiometargeted therapies for uveitis. Dysbiosis may promote uveitis through antigenic mimicry, T-cell imbalance, increased intestinal permeability, and reduced production of anti-inflammatory metabolites, including short-chain fatty acids (SCFA) and secondary bile acids (SBA). Secondary bile acids, such as deoxycholic acid, attenuate experimental autoimmune uveitis by inhibiting dendritic cell NF-κB signaling via TGR5/cAMP-PKA pathways, while reduced bile acid pools are observed in disease models. Antibiotic-induced microbiome perturbation shows bidirectional effects, with short-term depletion delaying uveitis but prolonged depletion disrupting immune regulation. Probiotics and prebiotics demonstrate anti-inflammatory effects in experimental models, with E. coli Nissle 1917 reducing disease severity and limited human data suggesting fewer uveitis recurrences. Fecal microbiota transplantation (FMT) shows potential benefit in small, heterogeneous uveitis studies and is supported by efficacy in gastrointestinal inflammatory diseases. Available data support a biologically plausible gut–eye axis in uveitis, but clinical applicability remains limited by small sample sizes, heterogeneous interventions, and short follow-up. Reviews emphasize the need for controlled trials that assess immune and metabolic markers, while using precise approaches to better define treatment effects and reduce the risk of unintended immune responses. Emerging genetic and causal inference studies may aid in identifying relevant microbial targets, though clinical validation is required. Microbiome-targeted therapies for uveitis are supported by mechanistic rationale and promising preclinical evidence, with early clinical signals from probiotics, dietary modulation, and FMT. However, robust randomized trials are required before integration into routine uveitis management.

Inherited retinal dystrophies (IRDs) in children are rare genetic disorders causing early-onset visual impairment. Recent advances in gene therapy have led to one approved treatment and multiple early-phase trials showing acceptable safety and functional improvement. Early intervention during childhood is considered critical due to greater retinal plasticity and residual photoreceptor viability. A systematic literature review of PubMed-indexed studies published between 2021 and 2025 was conducted to evaluate gene therapy advances in pediatric IRDs. Voretigene neparvovec (Luxturna) for RPE65-associated IRD demonstrated durable improvements in light sensitivity and functional vision lasting up to 3–4 years. Real-world pediatric data confirmed gains in full-field stimulus testing and visual fields, with modest visual acuity improvement. Adverse events were mainly procedurerelated, including intraocular pressure elevation, inflammation, and localized chorioretinal atrophy, underscoring the need for long-term follow-up. Emerging trials include in vivo CRISPR-based therapy for CEP290-associated Leber congenital amaurosis with acceptable safety and functional improvement in most patients, and gene supplementation for CNGB3-associated achromatopsia showing good tolerability but variable efficacy. Additional AAV-based approaches for choroideremia and retinitis pigmentosa are under investigation, supported by advances in vector design and delivery systems targeting pediatric IRDs. Current evidence indicates that gene therapy for pediatric IRDs is generally safe and can improve functional vision, particularly light sensitivity and navigation. However, treatment responses vary, and visual acuity improvements are often limited. Meta-analyses highlight heterogeneity across trials and the need for standardized pediatric outcome measures. Earlier treatment appears to yield better functional outcomes but requires careful monitoring for inflammation and injectionrelated complications. Gene therapy has entered clinical practice for pediatric IRDs and continues to expand through innovative molecular and delivery approaches. While early functional gains and safety signals are encouraging, long-term efficacy, durability, and safety must be established through ongoing trials, and optimized pediatric outcome measures.

Diabetic retinopathy (DR) is the leading cause of preventable blindness in working-age adults worldwide, affecting approximately one-third of the 537 million people living with diabetes. This number is expected to rise to 783 million by 2045. As diabetes prevalence increases, so does the socio-economic burden of diabetes-related vision loss. Despite major advances in treatment, significant gaps remain in early detection, treatment effectiveness, and access to care. This review discusses recent research on the pathogenesis and current clinical management of DR. DR develops as a result of prolonged chronic hyperglycemia and progresses through four major pathways: activation of the polyol pathway, formation of advanced glycation end products (AGEs), activation of protein kinase C, and increased flux through the hexosamine pathway. These mechanisms lead to oxidative stress, endothelial damage, loss of pericytes, leukocyte adhesion, increased inflammatory signaling, and chronic low-grade inflammation. Retinal neurodegeneration, including ganglion cell loss and Müller cell activation, often precedes visible vascular changes, resulting in early injury to the neurovascular unit. Breakdown of the blood–retina barrier causes diabetic macular edema (DME), while retinal ischemia can trigger pathological neovascularization in proliferative DR (PDR). Early management focuses on systemic risk-factor control, including HbA1c <7%, blood pressure <130/80 mmHg, and optimized lipid levels. Intravitreal anti-VEGF agents are first-line therapy for center-involving DME and PDR, with studies showing 30–40% of patients achieving a three-line visual acuity improvement. Panretinal photocoagulation remains the gold standard for high-risk PDR, while intravitreal corticosteroids are used for DME resistant to anti-VEGF therapy. Vitrectomy is reserved for non-clearing vitreous hemorrhage, tractional retinal detachment, or refractory edema. Overall, DR is now recognized as a neurovascular-inflammatory disease, underscoring the importance of early multidisciplinary care to prevent blindness, reduce treatment burden, and improve quality of life for individuals with diabetes.

To investigate the characteristics of referral for glaucoma surgery and compare surgical practices in various European regions in 2025.

Subhialoidinė kraujosruva - tai reta, tačiau regai pavojinga būklė, galinti pasireikšti nėštumo laikotarpiu dėl Valsalvos retinopatijos. Staigus intratorakalinio arba intraabdominalinio spaudimo padidėjimas gali sukelti tinklainės kapiliarų plyšimą ir kraujo susikaupimą geltonosios dėmės srityje. Aprašomas 27 metų moters subhialoidinės kraujosruvos atvejis, pasireiškęs 33 nėštumo savaitę po vėmimo epizodo. Laiku atlikus Nd:YAG lazerinę hialoidotomiją, rega reikšmingai pagerėjo. Gimdymo taktika parinkta individualiai, įvertinus pakartotinio kraujavimo riziką.

This study examines five circulating microRNAs (miRNAs) (miR-29a, let-7i, miR-204, miR-142, and miR-328) potentially relevant to the diagnostic and/or prognostic significance of myopia. miRNA expression was analyzed using StepOnePlus™ RT-PCR. miRNA expression was evaluated in whole blood samples collected and stored using Tempus™ Blood RNA Tubes. The expression of five miRNAs was analyzed in 88 participants: 45 in the myopia group and 43 in the control (emmetropic) group. Heatmap analysis revealed differences in the expression patterns of miR-29a, let-7i, miR-204, and miR-142 when comparing individuals with myopia and controls. The intensity of miR-328 expression was similar between the myopia and control groups. A significant correlation was observed between miR-204 ΔCt and spherical equivalent. However, comparison of median values between different degrees of myopia and the control group did not reveal significant differences. The simultaneous evaluation of multiple circulating miRNAs may help to better understand biological processes associated with myopia.

Since age-related macular degeneration (AMD) is the leading cause of irreversible central vision loss in the aging population, it is a significant global health concern. Although anti-vascular endothelial growth factor (anti-VEGF) treatments are effective, not all patients respond to them fully. This study focuses on key single-nucleotide variants in the CXCL8 (rs2227306), MAP3K7 (rs157432), LTA/TNF (rs2229094), EXOC3L1 (rs868213), PROCR (rs867186), TRAF2 (rs10781522), and serum levels of these genes in AMD development and treatment response. It examines the genetic factors associated with susceptibility to AMD and how they influence response to therapy. The study investigates the relationships between specific genetic variations, serum protein levels, and both exudative and early AMD, as well as responses to anti-VEGF treatment. These findings may help guide risk assessment and personalized AMD therapies.

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.