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Background Form-deprivation myopia (FDM) in chicks is one of the key models for studying myopia development. The specific molecular events and activation dynamics within the retina during early FDM stage in chicks remain unclear. Methods Retinal transcriptome datasets (GSE161497, GSE227724) were analyzed using DESeq2 and edgeR to identify differentially expressed genes (DEGs). Protein-protein interaction networks were constructed and visualized, with hub genes identified via the Maximal Clique Centrality algorithm. Functional enrichment was analyzed. Western Blot was used to validate β-catenin and phospho-β-catenin protein expression in control, FDM 1d, and FDM 5d chick retinas. Results Analysis revealed 36 common DEGs between DESeq2 and edgeR. PPI network analysis identified CTNNB1 (β-catenin), GNAQ, and TSHR as the top three hub genes. Western Blot demonstrated significant and sustained upregulation of both total β-catenin and phospho-β-catenin protein levels in FDM 1d and FDM 5d retinas compared to controls, with peak expression at FDM 5d within observed time. Conclusion This study provides evidence of sustained activation of the Wnt/β-catenin signaling pathway specifically within the chick retina during early FDM development, highlighted by CTNNB1 as a top hub gene and confirmed by progressive increases in both total and activated β-catenin protein. This suggests a potentially conserved role for retinal Wnt/β-catenin signaling in myopia pathogenesis.

Altered expressions of pro-/anti-oxidant genes are known to regulate the pathophysiology of obstructive sleep apnea (OSA).We aim to explore the role of a novel long non-coding (lnc) RNA FKSG29 in the development of intermittent hypoxia with re-oxygenation (IHR)-induced endothelial dysfunction in OSA. Gene expression levels of key pro-/anti-oxidant genes, vasoactive genes, and the FKSG29 were measured in peripheral blood mononuclear cells from 12 subjects with primary snoring (PS) and 36 OSA patients. Human monocytic THP-1 cells and human umbilical vein endothelial cells (HUVEC) were used for gene knockout and double luciferase under IHR exposure. Gene expression levels of the FKSG29 lncRNA, NOX2, NOX5, and VEGFA genes were increased in OSA patients versus PS subjects, while SOD2 and VEGFB gene expressions were decreased. Subgroup analysis showed that gene expression of the miR-23a-3p, an endogenous competitive microRNA of the FKSG29, was decreased in sleep-disordered breathing patients with hypertension versus those without hypertension. In vitro IHR experiments showed that knock-down of the FKSG29 reversed IHR-induced ROS overt production, early apoptosis, up-regulations of the HIF1A/HIF2A/NOX2/NOX4/NOX5/VEGFA/VEGFB genes, and down-regulations of the VEGFB/SOD2 genes, while the protective effects of FKSG29 knock-down were abolished by miR-23a-3p knock-down. Dual-luciferase reporter assays confirmed that FKSG29 was a sponge of miR-23a-3p, which regulated IL6R directly. Immunofluorescence stain further demonstrated that FKSGH29 knock-down decreased IHR-induced uptake of oxidized low density lipoprotein and reversed IHR-induced IL6R/STAT3/GATA6/ICAM1/VCAM1 up-regulations. The findings indicate that the combined RNA interference may be a novel therapy for OSA-related endothelial dysfunction via regulating pro-/anti-oxidant imbalance or targeting miR-23a-IL6R-ICAM1/VCAM1 signaling.

This study aimed to study the impact of a combination of maternal and post-weaning high-fat diets and whether resveratrol was beneficial. Sprague-Dawley dams were fed either chow or a high-fat diet, before mating, during pregnancy, and into lactation. At weaning, their offspring were randomly fed chow or a high-fat diet. Four experimental groups were generated: CC (maternal/postnatal chow diet), HC (maternal high-fat/postnatal chow diet), CH (maternal chow/postnatal high-fat diet), and HH (maternal/postnatal high-fat diet). A fifth group consisted of HH plus resveratrol. The 4 month-old offspring of HH group had higher body weight, higher levels of plasma triglycerides, leptin, angiotensin I and angiotensin II and abnormal intraperitoneal glucose tolerance test results, which fulfilled the features of metabolic syndrome. The dysregulation of the renin-angiotensin system was seen in multiple organs. Sirtuin 1 expression/abundance was reduced by a maternal/postnatal high-fat diet, in all the organs examined. Resveratrol ameliorated most of the features of metabolic syndrome and molecular alterations. The administration of a high-fat diet in both periods showed interactive metabolic effects in the plasma and many organs. Our results suggest that a maternal high-fat diet sensitizes offspring to the adverse effects of subsequent high-fat intake on multiple organs.

Background Nonalcoholic fatty liver disease (NAFLD) can develop in prenatal stages and can be exacerbated by exposure to a postnatal high-fat (HF) diet. We investigated the protective effects of resveratrol on prenatal and postnatal HF diet-induced NAFLD. Methods Male Sprague–Dawley rat offspring were placed in five experimental groups ( n  = 10–12 per group): normal diet (VNF), maternal HF diet (ONF), postnatal HF diet (VHF), and maternal HF diet/postnatal HF diet (OHF). A therapeutic group with resveratrol for maternal HF diet/postnatal HF diet (OHFR) was used for comparison. Resveratrol (50 mg/kg/day) was dissolved in drinking water for offspring from post-weaning to postnatal day (PND) 120. Results We found that HF/HF-induced NAFLD was prevented in adult offspring by the administration of resveratrol. Resveratrol administration mediated a protective effect on rats on HF/HF by regulating lipid metabolism, reducing oxidative stress and apoptosis, restoring nutrient-sensing pathways by increasing Sirt1 and leptin expression, and mediating the renin-angiotensin system (RAS) to decrease angiotensinogen, renin, ACE1, and AT1R levels and increased ACE2, AT2R and MAS1 levels compared to those in the OHF group. Conclusion Our results suggest that a maternal and post-weaning HF diet increases liver steatosis and apoptosis via the RAS. Resveratrol might serve as a therapeutic target by mediating protective actions against NAFLD in offspring exposed to a combination of maternal and postnatal HF diet.

This study aimed to analyze the impact of long-term ICL implantation on lens density, focusing on the relationship between the anterior subcapsule, anterior lens density, and implantable collamer lenses (ICL) position after ICL V4c implantation. This retrospective study included 145 eyes with ICL V4c implantation and average follow-up of 4.2 years (range: 3-8 years). The control group comprised 65 myopic eyes without surgery. All participants underwent comprehensive ophthalmologic examinations, and lens density were measured using quantitative Scheimpflug images. The central anterior subcapsular densities were 8.62 ± 1.39% preoperatively, 8.99 ± 1.31% at 3 months, and 9.29 ± 0.95% at the last follow-up post ICL implantation (p < 0.001). At last follow-up, the anterior subcapsular densities were 9.29 ± 0.95% in the central region, 8.92 ± 0.79% in the long axis of peripheral region, and 8.62 ± 0.76% in the short axis of peripheral region (p < 0.001). The densities were lower in the non-surgical group than in the ICL implantation group. One eye (0.69%) was discovered to have anterior subcapsular and nuclear opacification. The density of the anterior subcapsule increased over time after ICL implantation. Preoperative refraction and pupil size were correlated with changes in anterior subcapsule density. The central anterior subcapsule density was higher than that at the periphery, and the peripheral density of the long axis was higher than that of the short axis.

Prenatal high-fat diet (HFD) or exposure to microplastics can affect the accumulation of liver fat in offspring. We sought to determine the effects of maternal HFD intake and microplastic exposure on fatty liver injury through oxidative stress in pups. Pregnant female Sprague–Dawley rats were randomly divided into maternal HFD (experimental group) or normal control diet (NCD; control group) groups with or without microplastic exposure. As a result, the following groups were established: HFD-L (HFD + microplastics, 5 µm, 100 μg/L), HFD-H (HFD + microplastics, 5 µm, 1000 μg/L), NCD-L (NCD + microplastics, 5 µm, 100 μg/L), and NCD-H (NCD + microplastics, 5 µm, 1000 μg/L). The pups were sacrificed on postnatal day 7 (PD7). Liver histology revealed increased hepatic lipid accumulation in pups in the HFD-L and HFD-H groups compared to those in the HFD, NCD-L, NCD-H, and NCD groups on PD7. Similarly, liver TUNEL staining and cellular apoptosis were found to increase in pups in the HFD-L and HFD-H groups compared to those in the HFD, NCD-L, NCD-H, and NCD groups. The expression levels of malondialdehyde, a lipid peroxidation marker, were high in the HFD, HFD-L, and HFD-H groups; however, the highest expression was observed in the HFD-H group (p < 0.05). The levels of glutathione peroxidase, an antioxidant enzyme, decreased in the HFD, HFD-L, and HFD-H groups (p < 0.05). Overall, oxidative stress with cellular apoptosis plays a vital role in liver injury in offspring after maternal intake of HFD and exposure to microplastic; such findings may shed light on future therapeutic strategies.

A multi-step procedure was effectively employed to synthesize innovative three-dimensional (3D) heterostructures encompassing sodium titanate (Na2Ti3O7) nanowire cores, an intermediate resorcinol–formaldehyde (RF) layer, and outer silver (Ag) nanoparticle sheaths, referred to as Na2Ti3O7@RF@Ag heterostructures. Initially, a one-step hydrothermal technique facilitated the direct growth of single-crystal Na2Ti3O7 nanowires onto a flexible Ti foil. Subsequently, a two-step wet chemical process facilitated the sequential deposition of an RF layer and Ag nanoparticles onto the Na2Ti3O7 nanowires at a low reaction temperature. Optimal concentrations of silver nitrate and L-ascorbic acid can lead to the cultivation of Na2Ti3O7@RF@Ag heterostructures exhibiting heightened surface-enhanced Raman scattering (SERS), which is particularly beneficial for the detection of rhodamine B (RhB) molecules. This phenomenon can be ascribed to the distinctive geometry of the Na2Ti3O7@RF@Ag heterostructures, which offer an increased number of hot spots and surface-active sites, thereby showcasing notable SERS enhancement, commendable reproducibility, and enduring stability over the long term. Furthermore, the Na2Ti3O7@RF@Ag heterostructures demonstrate remarkable follow-up as first-order chemical kinetic and recyclable photocatalysts for the photodecomposition of an RhB solution under UV light irradiation. This result can be attributed to the enhanced inhibition of electron–hole pair recombination and increased surface-active sites.

Hypertension can originate from early-life exposure to oxidative stress. As reported, dimethyl fumarate (DMF) activates nuclear factor erythroid-derived 2-related factor 2 (Nrf2) and protects against oxidative stress damage. We examined whether maternal DMF therapy protects adult offspring against hypertension programmed by prenatal dexamethasone (DEX) and postnatal high-fat (HF) diet exposure. We examined male Sprague Dawley rat offspring at 4 months of age from five groups (n = 11–13/group): control, DEX (0.1mg/kg i.p. from gestational day 16 to 22), HF (D12331 diet from weaning to 16 weeks of age), DEX+HF, and DEX+HF+DMF (50mg/kg/day via gastric gavage for 3 weeks during pregnancy). Maternal DMF therapy prevented male offspring against hypertension programmed by combined DEX and HF exposures. The protective effects of maternal DMF include reduced oxidative stress, decreased plasma asymmetric dimethylarginine (ADMA) levels, downregulated the renin-angiotensin system (i.e. Ren, Agt, Ace, and Agtr1a), increased renal protein levels of certain nutrient-sensing signals, and promoted autophagy. In conclusion, maternal Nrf2 activation by DMF protects male adult offspring against hypertension programmed by combined DEX and HF exposures. Our results cast a new light on the therapeutic potential of targeting Nrf2 signaling pathway as reprogramming strategies to prevent programmed hypertension in children exposed to antenatal corticosteroids and postnatally excessive consumption of fat.

Ischaemic heart disease remains a leading cause of mortality worldwide, highlighting the need for new agents that protect vascular function. Tectorigenin, a plant-derived isoflavone, is known for its anti-inflammatory and antioxidant properties, but its direct effects on vascular tone have not been clearly explored. This study investigated the vasorelaxant actions of tectorigenin in endothelium-denuded porcine coronary arteries and examined the mechanisms involved. Using isolated artery rings pre-contracted with a thromboxane A₂ analogue, we found that tectorigenin induced concentration-dependent relaxation with an EC₅₀ of approximately 11 µM. Pharmacological inhibition experiments revealed that relaxation at 10–30 µM was significantly reduced by oestrogen receptor antagonists and by 4-aminopyridine, a blocker of voltage-gated potassium channels, and was completely abolished under high-potassium conditions. In contrast, inhibitors targeting neural conduction, nitric oxide synthase, cyclic nucleotide pathways, and other potassium channels had no significant impact. Immunohistochemistry and qPCR analyses indicated predominant ERα expression in the coronary arteries. These findings are consistent with contributions from oestrogen receptors (with ERα predominance) and 4-AP-sensitive Kv channels to the relaxant response; a direct ER-Kv coupling was not established in this ex vivo model. This is the first study to characterise the vascular pharmacology of tectorigenin in a large-animal coronary model. Further in vivo investigations are warranted to assess its potential in managing cardiovascular diseases.

Studies in experimental animals show transmissibility of amyloidogenic proteins associated with prion diseases, Alzheimer's disease, Parkinson's disease, and other neurodegenerative diseases. Although these data raise potential concerns for public health, convincing evidence for human iatrogenic transmission only exists for prions and amyloid β after systemic injections of contaminated growth hormone extracts or dura mater grafts derived from cadavers. Even though these procedures are now obsolete, some reports raise the possibility of iatrogenic transmission of amyloid β through putatively contaminated neurosurgical equipment. Iatrogenic transmission of amyloid β might lead to amyloid deposition in the brain parenchyma and blood vessel walls, potentially resulting in cerebral amyloid angiopathy after several decades. Cerebral amyloid angiopathy can cause life-threatening brain haemorrhages; yet, there is no proof that the transmission of amyloid β can also lead to Alzheimer's dementia. Large, long-term epidemiological studies and sensitive, cost-efficient tools to detect amyloid are needed to better understand any potential routes of amyloid β transmission and to clarify whether other similar proteopathic seeds, such as tau or α-synuclein, can also be transferred iatrogenically.