Notes

The consequence involving Meibomian Glandular Dysfunction Treatment method about Rest Good quality.
To investigate the effects and mechanism of β-elemene on the expressions of hypoxia-inducible factor-1α (HIF-lα), vascular endothelial growth factor (VEGF) and inducible nitric oxide synthase (iNOS) in human retinal pigment epithelial (RPE) cells under high glucose conditions.

ARPE-19 cell line was cultured under eight conditions 1) low glucose (LG; 5.5 mmol/L); 2) high glucose (HG; 33 mmol/L); 3) high glucose with 20 µg/mL β-elemene (HG+20E); 4) high glucose with 40 µg/mL β-elemene (HG+40E); 5) high glucose with SB203590 [HG+SB203590, p38-mitogen-activated protein kinase (p38-MAPK) pathway inhibitor]; 6) high glucose with LY294002 [HG+LY294002, phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) pathway inhibitor]; 7) high glucose with 40 µg/mL β-elemene and SB203590 (HG+40E+SB203590); and 8) high glucose with 40 µg/mL β-elemene and LY294002 (HG+40E+LY294002). Cells were treated in conditions 1-4 for 24 and 48h, while for 48h in conditions 5-8. Then mRNA and protein levels of HIF-1α, VEGF and iNOS in ckt signaling pathways may play a role in this inhibitory effect.
β-elemene down-regulates HIF-1α, VEGF and iNOS in ARPE-19 cells under a high glucose condition. The inhibitory effect of β-elemene is more significant when its concentration and treatment time are increased, as well as it is combined with SB203590 or LY294002 treatment. P38-MAPK and PI3K/Akt signaling pathways may play a role in this inhibitory effect.
To determine whether Houttuynia cordata Thunb (HCT) can increase the survival of the retinal ganglion cells (RGCs) and inhibit microglia activation following retinal ischemia-reperfusion (RIR) injury.

Rat model of RIR was induced by transient elevation of the intraocular pressure (IOP). HCT was orally administered for 2d before the performance of retinal RIR model and once a day for the next 14d. After 14d of RIR injury, the rats were sacrificed for further analysis. Survival RGCs were stained with haematoxylin and eosin (H&E). Apoptosis of RGCs was detected by TUNEL staining. Retinal function was examined by flash-electroretinography (F-ERG). Retinal microglia were labeled using Iba-1, one specific marker for microglia. The mRNA expression levels of inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNF-α), and interleukin 1 beta (IL-1β) were assessed by quantitative real time reverse transcription polymerase chain reaction (qRT-PCR).

Systemic HCT treatment significantly reduced RGCs death by H&E staining and exhibited an anti-apoptotic effect as assessed by TUNEL staining at day 14 after RIR injury. HCT greatly improved the retinal function as examined by F-ERG. The number of activated microglia significantly increased after RIR injury, which was significantly attenuated by HCT treatment. Besides, RIR injury induced a strong upregulation of pro-inflammatory genes TNF-α, iNOS and IL-1β mRNAs at day 14 post injury, which was suppressed by HCT.

Neuroprotective effects of HCT encourage the survival of RGCs through inhibiting microglia activation due to RIR injury. Together these results support the use of HCT as promising therapy for the ischemic events of the retina diseases.
Neuroprotective effects of HCT encourage the survival of RGCs through inhibiting microglia activation due to RIR injury. Together these results support the use of HCT as promising therapy for the ischemic events of the retina diseases.
To find a new concept to show whether or not apoptosis of retinal ganglion cells (RGCs) can be determined in the histology of acute hyperglycemia in the role of expressed Brn3b gene related to nitric oxide (NO), caspase-3, nuclear factor kappa-B (NF-κB), and tumor necrosis factor-α (TNF-α) as an early predictor of primary open angle glaucoma (POAG) eyes and their associations.

Experimental
study was carried out using adult male, white Sprague-Dawley rats aged ≥2mo, weighing 150-200 g. The animals were divided into two groups, one group receiving intraperitoneal injection of streptozotociz 50 mg/kg in 0.01 mol/L citric buffer and pH 4.5 and a comparison made with the control group. Retinal tissue was divided into two parts (both experimental and control groups respectively) a) right retina for immunohistochemistry (IHC; caspase-3 and TNF-α); b) left retina was divided into two parts for the purpose of real-time polymerase chain reaction (PCR) test (RNA extraction for Brn3b gene expression analysis) and ELISA test (NO and NF-κB).

The experimental group showed a decrease in Brn3b gene expression compared to the control group (1.3-fold lower in 2
month; 1.1-fold lower in 4
month and 2.5-fold lower in 6
month). However, there was a decrease of NO, caspase-3, and an increase of NF-κB and TNF-α quantity.

The expression of mRNA Brn3b gene is inversely proportional to apoptosis in RGCs. The quantity of NO, caspase-3, NF-κB and TNF-α is influential in expression of Brn3b in RGCs caused by hyperglycemia in diabetic rats.
The expression of mRNA Brn3b gene is inversely proportional to apoptosis in RGCs. The quantity of NO, caspase-3, NF-κB and TNF-α is influential in expression of Brn3b in RGCs caused by hyperglycemia in diabetic rats.
To compare the differences in kinetics, distribution, and toxicity of triamcinolone acetonide (TA) between the injection methods, sub-Tenon and intravitreal injections in rabbit ocular tissues.

TA was injected into the vitreous or the sub-Tenon in rabbits. For pharmacokinetic study, rabbits were sacrificed periodically and then TA in blood and ocular tissues (retina/choroids, vitreous, and aqueous humor) were measured over 91d. For toxicological study, clinical signs, slit-lamp microscopic examination, ophthalmological test were performed. The eyeballs and surrounding tissues were collected and fixed with glutaraldehyde-formalin solution, and then paraffin embedded for histological investigation.

Higher levels of TA were distributed in the intraocular tissues when injected into the vitreous compared to the sub-Tenon. Conversely, TA level was remarkably lower in the rabbits which received intravitreal TA injections than those treated with sub-Tenon injection throughout the study period in plasma. Opticalma, between the two injection methods. Although further study is needed to explain the species difference between human and rabbit, it is assumed that the difference in the frequency of intraocular pressure elevation and cataract formation by TA between the two injection methods are directly related to the TA concentrations in aqueous humor and vitreous body in each injection methods. Systemic toxicity and technic-associated toxicity are also closely related to kinetics of TA in plasma and each injection method itself, respectively.
To investigate the phototoxic effect of long-term excessive narrow-band blue light in staurosporine-induced differentiated retinal ganglion cells-5 (SSRGC-5).

SSRGC-5 cells were divided into two groups, blue light group (BL group) and control group. Cell viability was assessed by using CCK-8 assay. Metabolic profile analysis was performed by using Seahorse extracellular flux analyzer. Mitochondria ultrastructure were studied
transmission electron microscope (TEM). Mitochondria contents and oxidative stress was evaluated by flow cytometry. Western blotting was performed to monitor the changes in mitogen-activated protein kinases (MAPK) pathway and PI3K/AKT pathway.

Blue light caused morphological changes of SSRGC-5 cells. The cell viability was significantly decreased from 3h in BL group. Intercellular ROS and mitochondrial superoxide levels were increased following blue light exposure. Metabolic profiling identified blue light induced SSRGC-5 cells to have severely compromised mitochondrial function. This was accompanied by impaired mitochondrial ultrastructure and remodeling, increased expression of the mitochondrial related proteins, and increased glycolysis as compensation. Moreover, the results showed that blue light induced higher expression of p-p38, p38, p-JNK, p-ERK, p-c-Jun, c-Jun, and p-AKT.

These findings indicate that excessive narrow-band blue light induces oxidative stress and mitochondrial metabolic remodeling dysregulate in SSRGC-5 cells. USP25/28 inhibitor AZ1 Activated MAPK and AKT signaling pathways are involved in this process.
These findings indicate that excessive narrow-band blue light induces oxidative stress and mitochondrial metabolic remodeling dysregulate in SSRGC-5 cells. Activated MAPK and AKT signaling pathways are involved in this process.
To analyze the retinal proteomes with and without conbercept treatments in mice with oxygen-induced retinopathy (OIR) and identify proteins involved in the molecular mechanisms mediated by conbercept.

OIR was induced in fifty-six C57BL/6J mouse pups and randomly divided into four groups. Group 1 Normal17 (
=7), mice without OIR and treated with normal air. Group 2 OIR12/EXP1 (
=14), mice received 75% oxygen from postnatal day (P) 7 to 12. Group 3 OIR17/Control (
=14), mice received 75% oxygen from P7 to P12 and then normal air to P17. Group 4 Lang17/EXP2 (
=21), mice received 75% oxygen from P7 to P12 with intravitreal injection of 1 µL conbercept at the concentration of 10 mg/mL at P12, and then normal air from P12 to P17. Liquid Chromatography-Mass Spectrometry (LC-MS)/MS data were reviewed to find proteins that were up-regulated after the conbercept treatment. Gene ontology (GO) analysis was performed of conbercept-mediated changes in proteins involved in single-organism processes, biological regulation, cellular processes, immune responses, metabolic processes, locomotion and multiple-organism processes.

Conbercept induced a reversal of hypoxia-inducible factor 1 signaling pathway as revealed by the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis and also induced down-regulation of proteins involved in blood coagulation and fibrin clot formation as demonstrated by the Database for Annotation, Visualization and Integrated Discovery (DAVID) and the stimulation of interferon genes studies. These appear to be risk factors of retinal fibrosis. Additional conbercept-specific fibrosis risk factors were also identified and may serve as therapeutic targets for fibrosis.

Our studies reveal that many novel proteins are differentially regulated by conbercept. The new insights may warrant a valuable resource for conbercept treatment.
Our studies reveal that many novel proteins are differentially regulated by conbercept. The new insights may warrant a valuable resource for conbercept treatment.The use of personal protective equipment (PPE) for ophthalmologists caring for asymptomatic patients remains controversial. This commentary reviews the latest emerging evidence. This is paramountly important in shaping health policies in countries which is not currently recommended.•We have developed a framework to describe the dynamics of Functional Connectivity (dFC) estimated from brain activity time-series as a complex random walk in the space of possible functional networks. This conceptual and methodological framework considers dFC as a smooth reconfiguration process, combining "liquid" and "coordinated" aspects. Unlike other previous approaches, our method does not require the explicit extraction of discrete connectivity states.•In our previous work, we introduced several metrics for the quantitative characterization of the dFC random walk. First, dFC speed analyses extract the distribution of the time-resolved rate of reconfiguration of FC along time. These distributions have a clear peak (typical dFC speed, that can already serve as a biomarker) and fat tails (denoting deviations from Gaussianity that can be detected by suitable scaling analyses of FC network streams). Second, meta-connectivity (MC) analyses identify groups of functional links whose fluctuations co-vary in time and that define veritable dFC modules organized along specific dFC meta-hub controllers (differing from conventional FC modules and hubs).
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