Search Results (102)

The internal mammary arteries (IMAs) and coronary arteries share many common characteristics. The inner layer (tunica intima, or intima) of both arteries is lined with a smooth, longitudinally orientated monolayer of endothelial cells (ECs), connective tissue, and an internal elastic lamina that separates the tunica intima from the tunica media (middle layer). The intima of IMAs is lined with an additional protective layer, the neointima, containing vascular smooth muscle cells (VSMCs). The neointima, located between the intima and internal elastic lamina, protects IMAs from damage by assisting in the remodeling of VSMCs. Coarse longitudinal folds in the internal elastic lamina of IMAs partially prevent the infiltration of VSMCs into damaged IMAs, and intimal thickening is thus less likely to occur. Inflamed IMAs resist the migration of monocytes across the endothelial layer and prevent the formation of lipid-rich macrophages (foam cells) within the subintimal or medial layers of arteries. IMAs are thus less likely to form plaques and develop atherosclerosis (AS). Higher levels of prostacyclin (PGI2) in IMAs prevent blood clotting. The anti-thrombotic agents, and production of tumor necrosis factor α (TNF-α), interferon-γ (INF-γ), and visfatin render IMAs more resistant to inflammation. An increase in the production of nitric oxide (NO) by ECs of IMAs may be due to small ubiquitin-like modifier (SUMO) proteins that alter the nuclear factor kappa B (NF-κB) and TLR pathways. The production of reactive oxygen species (ROS) in IMAs is suppressed due to the inhibition of NADPH oxidase (NOX) by a pigment epithelium-derived factor (PEDF), which is a serine protease inhibitor (SERPIN). In this review, a comparison is drawn between the anatomy of IMAs and coronary arteries, with an emphasis on how ECs of IMAs react to immunological changes, rendering them more suited for coronary artery bypass grafts (CABGs). This narrative review covers the most recent findings published in PubMed and Crossref databases. Full article

Retinal degeneration is associated with dietary factors and environmental light exposure. This study investigated the effects of a high-fructose high-fat (HFHF) diet on susceptibility to blue light (BL)-induced retinal damage. Male ICR mice were randomized into three groups: control, BL alone, and BL plus HFHF diet (BL + HFHF). The BL + HFHF group consumed the HFHF diet for 40 weeks, followed by 8 weeks of low-intensity BL exposure (465 nm, 37.7 lux, 0.8 μW/cm²) for 6 h daily. The BL group underwent the same BL exposure while kept on a standard diet. Histopathological analysis showed that, under BL exposure, the HFHF diet significantly reduced the number of photoreceptor nuclei and the thickness of the outer nuclear layer and inner/outer segments compared to the BL group (p < 0.05). While BL exposure alone caused oxidative DNA damage, rhodopsin loss, and Müller cell activation, the combination with an HFHF diet significantly amplified the oxidative DNA damage and Müller cell activation. Moreover, the HFHF diet increased blood–retinal barrier permeability and triggered apoptosis under BL exposure. Mechanistically, the BL + HFHF group exhibited increased retinal advanced glycated end product (AGE) deposition, accompanied by the activation of the receptor for AGE (RAGE), NFκB, and the NLRP3 inflammasome-dependent IL-1β pathway. In conclusion, this study underscores that unhealthy dietary factors, particularly those high in fructose and fat, may intensify the hazard of BL and adversely impact visual health. Full article

Dopaminergic amacrine cells (DACs) are a subclass of amacrine cells that modulate retinal processing and light adaptation by releasing dopamine. Although the role of dopamine is largely conserved, their retinal distribution across mammals remains incompletely characterized. In mice, rats, thirteen-lined ground squirrels (TLGSs), and macaques, we systematically compared the localization, number, and topography of DACs by their expression of tyrosine hydroxylase (TH), a crucial enzyme in the biosynthesis of dopamine. In all species examined, TH+ cells were primarily located in the inner nuclear layer; however, there was a species-dependent influence on their number and distribution. Mice exhibited the highest density of TH+cells but completely lacked displaced TH+cells (dTH+cells) in the ganglion cell layer. Despite interspecies variation in the total number of TH+cells in the retina, the overall density in rats, TLGSs, and macaques was similar. Most species displayed a higher density of DACs toward central retinal regions. However, rats exhibited a distinctive dorsal concentration, particularly among dTH+cells. Although most species examined exhibited a similar ratio of TH+cells to Brn3a+ retinal ganglion cells, TLGSs showed a marked reduction, indicating a potentially diminished dopaminergic modulatory role. Species-specific DAC topographies aligned with specialized visual regions, such as the visual streak in TLGS and the macula in macaques. These results reveal both conserved and divergent features of retinal dopamine circuitry, reflecting evolutionary adaptations to visual processing demands. Full article

Background/Objective: The Rs1 exon-1-del rat (Rs1KO) XLRS model shows normal retinal development until postnatal day 12 (P12) when small cystic spaces start to form in the inner nuclear layer. These enlarge rapidly, peak at P15, and then collapse by P19. These events overlap with eye opening at P12–P15. We investigated whether new light-driven retinal activity could contribute to the appearance and progression of schisis cavities in this rat model of XLRS disease. Methods: For dark rearing (D/D), mating pairs of Rs1KO strain were raised in total darkness in a special vivarium at UC Davis. When pups were born, they were maintained in total darkness, and eyes were collected at P12, P15, and P30 (n = 3/group) for each of the D/D and cyclic light-reared 12 h light–12 h dark (L/D) Rs1KO and wild-type (WT) littermates. Eyes were fixed, paraffin-embedded, and sectioned. Tissue morphology was examined by H&E and marker expression of retinoschisin1 (Rs1), rhodopsin (Rho), and postsynaptic protein 95 (Psd95) by fluorescent immunohistochemistry. H&E-stained images were analyzed with ImageJ version 1.54h to quantify cavity size using the “Analyze Particles” function. Results: Small intra-retinal schisis cavities begin to form by P12 in the inner retina of both D/D and L/D animals. Cavity formation was equivalent or more pronounced in D/D animals than in L/D animals. We compared Iba1 (activation marker of immune cells) distribution and found that by P12, when schisis appeared, Iba1⁺ cells had accumulated in regions of schisis. Iba1⁺ cells were more abundant in Rs1KO animals than WT animals and appeared slightly more prevalent in D/D- than L/D-reared Rs1KO animals. We compared photoreceptor development using Rho, Rs1, and Psd95 expression, and these were similar; however, the outer segments (OSs) of D/D animals with Rho labeling at P12 were longer than L/D animals. Conclusions: The results showed that cavities formed at the same time in D/D and L/D XLRS rat pups, indicating that the timing of schisis formation is not light stimulus-driven but rather appears to be a result of developmental events. Cavity size tended to be larger under dark-rearing conditions in D/D animals, which could be due to the decreased rate of phagocytosis by the RPE in the dark, allowing for continued growth of the OSs without the usual shedding of the distal tip, a key mechanism behind dark adaptation in the retina. These results highlight the complexity of XLRS pathology; however, we found no evidence that light-driven metabolic activity accounted for schisis cavity formation. Full article

Background/Objectives: This exploratory study aimed to assess the prevalence of retinal ischemic perivascular lesions (RIPLs) in individuals with cardiovascular disease (CVD) or associated risk factors and to investigate their potential role as non-invasive biomarkers of systemic ischemia using optical coherence tomography (OCT). Methods: A prospective observational study was conducted between July and October 2022. A total of 665 participants aged 40–90 years underwent macular OCT imaging using the Topcon Maestro 2 system. Participants were classified into two groups: those with ischemic CVD or risk factors (n = 297) and healthy individuals without cardiovascular conditions (n = 368). RIPLs were defined by inner nuclear layer thinning and outer nuclear layer expansion in perivascular regions and were identified by masked consensus of three independent evaluators. Results: The overall prevalence of RIPLs was 0.75% (five cases), exclusively observed in the diseased group (1.68%), with no cases identified among healthy individuals (p = 0.044). Stratified analysis showed an increase in RIPL prevalence with age, reaching 2.24% in the 70–79 years cohort. Statistically significant associations were found between RIPLs and hypertension, dyslipidemia, ischemic heart disease, and thrombosis (all p < 0.001). No significant association was observed with sex, myocardial infarction, or RIPL presence as an independent predictor (p = 0.08). Conclusions: Their identification through OCT during routine ophthalmologic examinations highlights a possible new avenue for early cardiovascular risk stratification. Nevertheless, the extremely low number of RIPL cases detected (only five out of six hundred and sixty-five participants; 0.75%) significantly limits the statistical power of the analysis and precludes strong conclusions. These findings should be regarded as preliminary and hypothesis-generating, requiring confirmation in larger, more diverse populations. Full article

Myo/Nog cells play a pivotal role in ocular development and demonstrate a rapid response to stress and injury. This study investigates their behavior and distribution in a murine model of retinitis pigmentosa, specifically in C3H/HeJ mice, which exhibit photoreceptor degeneration due to a homozygous mutation in the Pde6brd1 gene. Retinal samples from C3H/HeJ and C57BL/6J mice were analyzed at postnatal weeks 2.5 to 6 using hematoxylin and eosin staining, immunofluorescence for brain-specific angiogenesis inhibitor 1 (BAI1) expressed in Myo/Nog cells, and TUNEL labeling for apoptotic cell detection. The results demonstrated a progressive thinning of the outer nuclear layer (ONL) in C3H mice, accompanied by a significant increase in Myo/Nog cell numbers. In normal retinas, Myo/Nog cells were primarily located in the inner nuclear and outer plexiform layers. However, in C3H/HeJ mice, they accumulated in the ONL near apoptotic photoreceptors and within the choroid. Notably, in these degenerative regions, Myo/Nog cells exhibited features of phagocytosis, suggesting a role in apoptotic cell clearance. Additionally, parallels between Myo/Nog cell responses in retinitis pigmentosa and models of oxygen-induced retinopathy, ocular hypertension, and light damage suggest that these cells may be leveraged for therapeutic purposes. Full article

Passive films that form on Alloy 600 and Alloy 690 during four hours in simulated Primary Water (PW) of Pressurized Water Nuclear Reactors (PWRs) at 320 °C were investigated by in situ surface-enhanced Raman spectroscopy (SERS). Similar tests conducted on unalloyed nickel, unalloyed chromium, and laboratory alloys of Ni-10Cr, Ni-20Cr, Ni-5Cr-8Fe, and Ni-10Cr-8Fe aided in assigning the peaks in the surface-enhanced Raman (SER) spectra of the passive films of Alloy 600 and Alloy 690. SERS indicates an inner layer (IL) of Cr₂O₃/CrOOH forms on both Alloy 600 and Alloy 690 and that Alloy 690’s IL was more protective against corrosion due to its greater resistance to ion transport. The outer layer (OL) of Alloy 600 consists of NiO and spinels, FeCr₂O₄—M(Cr,Fe)₂O₄. The OL of Alloy 690 contains no spinel. A comparison of SER spectra in 320 °C PWR PW to the spectra following cooling down to room temperature and after exposure to air indicates some differences between in situ films and ex situ films. Full article

Zirconium alloys are essential materials for nuclear fuel cladding. During a loss-of-coolant accident (LOCA), zirconium alloy cladding can oxidize in high-temperature steam (>1000 °C), generating hydrogen and releasing significant heat. Without timely emergency actions, this can result in hydrogen explosions or nuclear leakage. In this study, titanium nitride (TiN), chromium (Cr), and TiN–Cr composite coatings were deposited on the surface of Zr-4 alloy using the magnetron sputtering method. The coatings’ surface and cross-sectional morphologies were examined using scanning electron microscopy (SEM), and their phase structures were analyzed with X-ray diffraction (XRD). The mechanical properties were evaluated using scratch tests, and their resistance to high-temperature steam oxidation was tested in a tube furnace connected to a steam generator. The results showed that the TiN, Cr, and TiN–Cr coatings exhibited strong adhesion to the Zr-4 substrates, with distinct interfaces and pure phase structures. After high-temperature steam oxidation, cracks appeared on the surfaces of the TiN, Cr, and TiN–Cr coatings, likely due to differences in the thermal expansion coefficients of TiO₂, Cr₂O₃, and residual Cr layers. These cracks created pathways for the oxidizing medium, potentially leading to the oxidation of the substrate or inner layers of the composite coatings. For the Cr and TiN–Cr coatings, despite cracking of the Cr layer and melting of the TiN layer at high temperatures, the residual Cr layer effectively restricted oxygen diffusion into the Zr-4 substrate. This study suggests that layers with low melting points, such as TiN, are unsuitable for composite coatings in high-temperature applications. However, adding a Cr layer on top of the TiN layer to form a TiN–Cr composite coating improves adhesion between the coating and the substrate. The TiN–Cr composite coating functions as an effective diffusion barrier at temperatures up to 1200 °C, comparable to a pure Cr coating. Full article

Paracentral acute middle maculopathy (PAMM) is a macular condition primarily detected using optical coherence tomography (OCT) imaging. It presents as hyperreflective bands within the inner nuclear layer (INL) of the retina, often leading to localized degenerative phenomena. PAMM is a condition that reveals a dysfunction in the microvascular network of the retina. However, it is not an isolated phenomenon but rather an indicator of deeper and even systemic, prevalently vascular-related issues related to a wide array of conditions that impact circulation, including retinal vein and artery occlusion, diabetic retinopathy, and hypertensive retinal vascular changes. PAMM occurs due to impaired perfusion within the retinal deep capillary plexus, clinically leading to subtle but noticeable blind spots (scotomas) in the central visual field. Recent advances in imaging technology, particularly optical coherence tomography angiography (OCTA), have provided a clearer view of the underlying vascular alterations. Thus, PAMM may currently serve as a biomarker in broader ocular and systemic pathologies before disease progression. This review explores the latest reports in the literature on PAMM, from its characteristic imaging features to the evolving theories behind its development. By bridging the gap between ophthalmology and systemic health, PAMM may facilitate earlier diagnosis and tailored management strategies for conditions that extend far beyond the eye. Understanding this entity could ultimately transform our approach to assessing vascular health toward further research, risk prediction, and patient care. Full article

The retinal structure is generally conserved across vertebrates; however, variations occur due to the relationship between environmental factors and visual perception. Birds have adapted to diverse ecological contexts, evolving specialized visual characteristics. In this study, we examined the retina of Audouin’s Gull (Larus audouinii) using light and transmission electron microscopy. This species is particularly intriguing as it is considered an outlier within the Laridae family: despite being a diurnal bird, it exhibits nocturnal/crepuscular foraging behaviour. Our analysis revealed a retina well adapted for diurnal activity, with features such as a retinal thickness comparable to that of other diurnal birds, a well-developed retinal pigment epithelium, and a high cone-to-rod density ratio. However, we also observed characteristics aligned with nocturnal or crepuscular activity, including a slightly increased rod density in central regions and the presence of two distinct types of horizontal cells in the inner nuclear layer. Additionally, the inner retina showed evidence of complex visual processing. These findings suggest that Audouin’s Gull is an excellent model for visual ecology studies due to its specialized adaptations. Full article

This study evaluated the neuroprotective potential of peptain-1 conjugated to a cell-penetrating peptide (CPP-P1) in an ocular hypertension model of glaucoma. Brown Norway (BN) rats were subjected to intraocular pressure (IOP) elevation via intracameral injection of silicone oil (SO), with concurrent intravitreal injections of either CPP-P1 or a vehicle. Retinal cross-sections were analyzed for markers of neuroprotection, including cAMP response element-binding protein (CREB), phosphorylated CREB (p-CREB), growth-associated protein-43 (GAP43), synapsin-1 (SYN1), and superoxide dismutase 2 (SOD2). Hematoxylin and eosin staining was used to assess retinal-layer thickness. SO-treated rats exhibited significant reductions in the thickness of the inner nuclear layer (INL, 41%, p = 0.016), inner plexiform layer (IPL, 52%, p = 0.0002), and ganglion cell layer (GCL, 57%, p = 0.001). CPP-P1 treatment mitigated these reductions, preserving INL thickness by 32% (p = 0.059), IPL by 19% (p = 0.119), and GCL by 31% (p = 0.057). Increased levels of CREB (p = 0.17) and p-CREB (p = 0.04) were observed in IOP-elevated, CPP-P1-treated retinas compared to IOP-elevated, vehicle-treated retinas. Although overall GAP43 levels were low, there was a modest increase in expression within the IPL and GCL in SO- and CPP-P1-treated retinas (p = 0.15 and p = 0.09, respectively) compared to SO- and vehicle-treated retinas. SO injection reduced SYN1 expression in both IPL and GCL (p = 0.01), whereas CPP-P1 treatment significantly increased SYN1 levels in the IPL (p = 0.03) and GCL (p = 0.002). While SOD2 expression in the GCL was minimal across all groups, a trend toward increased expression was observed in CPP-P1-treated animals (p = 0.16). The SO model was replicated with SO removal after 7 days and monitored for 21 days followed by retinal flat-mount preparation to assess retinal ganglion cell (RGC) survival. A 42% loss in RGCs (p = 0.009) was observed in SO-injected eyes, which were reduced by approximately 37% (p = 0.03) with CPP-P1 treatment. These findings suggest that CPP-P1 is a promising neuroprotective agent that promotes retinal ganglion cell survival and the preservation of other retinal neurons, potentially through enhanced CREB signaling in a rat model of SO-induced ocular hypertension. Full article

Background/Objective: The Rs1 exon-1-del rat (Rs1KO) XLRS model shows normal retinal development until postnatal day 12 (P12) when small cystic spaces start to form in the inner nuclear layer. These spaces enlarge rapidly, peak at P15, and then collapse by P19. Methods: We explored the possible involvement of Kir4.1 and Aqp4, the principal retina channels for water movement and homeostasis, along with Muller glia cells (MGCs), using semi-quantitative fluorescent immunohistochemistry at P7, P9, P12, and P30, in Rs1KO and WT littermates. Results: Kir4.1 expression was reduced in Rs1KO retinas at all the early time points—P7, P9, and P12—as the schisis cavities began to form; downregulation would reduce water egress from the retina. Aqp4 was upregulated at P30 in Rs1KO retinas during schisis cavity closure but not as cavities formed at P12. When examined by GFAP expression, MGCs were not activated at the preschisis P12 age but showed considerable GFAP expression at P30 following retinal cystic structural damage at P15, indicating that MGCs were activated during the period of retina water removal and cavity closure. Conclusions: The study results implicate the downregulation of Kir4.1 in schisis formation and a role for both Kir4.1 and Aqp4 upregulation in subsequent schisis closure. Full article

Age-related macular degeneration (AMD) is marked by a progressive loss of central vision and is the third leading cause of irreversible blindness worldwide. The exact mechanisms driving the progression of this macular degenerative condition remain elusive, and as of now, there are no available preventative measures for dry AMD. According to ancient records, ginseng affects the eyes by brightening them and enhancing wisdom. Modern pharmacological research shows that the active ingredients in ginseng, ginsenosides, may be used to prevent or improve eye diseases that threaten vision. Some articles have reported that ginsenoside Rg3 can treat diabetic retinopathy in mice, but no reports exist on its effects and mechanisms in AMD. Therefore, the role and mechanism of ginsenoside Rg3 in AMD warrant further study. This study aims to investigate the effects of Rg3 on AMD and its underlying molecular mechanisms. We established a mouse model of AMD to examine the impact of ginsenoside Rg3 on NaIO₃-induced apoptosis in the retina and to explore the related intrinsic mechanisms. The in vivo results indicated that ginsenoside Rg3 prevents NaIO₃-induced apoptosis in retinal pigment epithelial cells by inhibiting reactive oxygen species production and preventing the reduction in mitochondrial membrane potential. Additionally, we assessed the levels of protein expression within the apoptosis pathway. Ginsenoside Rg3 decreased the expression of Bax, cleaved caspase-3, and cleaved caspase-9 proteins. Additionally, it increased the expression of Bcl-2 by decreasing P-JNK levels. Moreover, our in vivo results showed that ginsenoside Rg3 enhanced retinal structure, increased the relative thickness of the retina, and decreased the extent of disorganization in both the inner and outer nuclear layers. Ginsenoside Rg3 may safeguard the retina against NaIO₃-induced cell apoptosis by attenuating reactive-oxygen-species-mediated mitochondrial dysfunction, in which the JNK signaling pathway is also involved. These findings suggest that ginsenoside Rg3 has the potential to prevent or attenuate the progression of AMD and other retinal pathologies associated with NaIO₃-mediated apoptosis. Full article

One of the challenges in energy supply for isolated power systems is maintaining a steady balance between generated and consumed energy. The application of energy storage systems and flexible energy sources is the most preferable approach for these systems. Small- and medium-sized nuclear power plants are promising, carbon-free options for energy supply to isolated power systems. However, these plants have low maneuverability. To solve this problem, this article discusses the use of a thermal accumulator using a phase change material (solar salt) to heat feedwater. Tubes with longitudinal fins are used to intensify heat transfer in the storage system. This paper presents a method for calculating heat transfer along the entire heat exchange surface of such an accumulator. A series of 2D simulations were conducted to study the solidification process of solar salt around a heat exchange tube at various temperatures on the inner wall surface. The regression dependences of heat transfer on the temperature of the inner surface of the wall and the thickness of the solid PCM layer were determined. Using the presented method and the obtained regression dependencies, we determined the time graphs of the temperature change in the heat transfer fluid at the outlet of the accumulator during discharge. Based on the results presented, it was found that an accumulator with 72.7 tons of solar salt (dimensions: 6 × 3.71 × 2.15 m) can replace a high-pressure heater №1 at a low-power nuclear power plant (50 MW) during 3450 s. Full article

BMI1, also known as B lymphoma Mo-MLV insertion region 1, is a protein in the Polycomb group that is implicated in various cellular processes, including stem cell self-renewal and the regulation of cellular senescence. BMI1 plays a role in the regulation of retinal progenitor cells and the renewal of adult neuronal cells. However, the presence, location, and quantification of BMI1 in the adult human eye have never previously been reported. In this study, we collected 45 frozen globes from eye banks, and ocular tissues were dissected. Protein was quantified by utilizing a custom electrochemiluminescence (ECL) assay developed to quantify the BMI1 protein. BMI1 was found in all ocular tissues at the following levels: the retina (1483.6 ± 191.7 pg/mL) and the RPE (296.4 ± 78.1 pg/mL). BMI1 expression was noted ubiquitously in the GCL (ganglion cell layer), the INL (inner nuclear layer), the ONL (outer nuclear layer), and the RPE (retinal pigment epithelium) via immunofluorescence, with higher levels in the inner than in the outer retinal layers and the RPE. These data confirm that BMI1 is expressed in the human retina. Further studies will illuminate the role that BMI1 plays in ocular cells. BMI1 levels are lower in aged retinas, possibly reflecting changes in retinal somatic and stem cell maintenance and disease susceptibility. Full article