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Effects of Aflibercept administration at 25 mg per kg body weight in retinas of mice subjected to the oxygen-induced retinopathy protocol

ABSTRACT: Effects of Aflibercept administration at 25 mg per kg body weight in retinas of mice subjected to the oxygen-induced retinopathy protocol

PROVIDER: PRJNA514455 | ENA |

REPOSITORIES: ENA

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Effects of Aflibercept administration at 25 mg per kg body weight in retinas of mice subjected to the oxygen-induced retinopathy protocol

Project description:We aimed at identifying the regulatory network of Aflibercept in the context of pathological neovascularization by using the oxygen-induced retinopathy mouse model as a surrogate of proliferative diabetic retinopathy Total RNA was collected from entire retinal cups dissected from mice subjected to the oxygen-induced retinopathy protocol and subsequently injected with Aflibercept either on postnatal day 13 (collection on day 14) or on postnatal day 13 and 15 (collection on day 17). Non-injected OIR littermates and age-matched mice housed in normoxic conditions were used as controls.

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Effects of Aflibercept administration at 25 mg per kg body weight in retinas of mice subjected to the oxygen-induced retinopathy protocol [P19]

Project description:We aimed at identifying the regulatory network of Aflibercept in the context of pathological neovascularization by using the oxygen-induced retinopathy mouse model as a surrogate of proliferative diabetic retinopathy Total RNA was collected from entire retinal cups dissected from 19-days old mice subjected to the oxygen-induced retinopathy protocol and subsequently injected with Aflibercept either on postnatal days 13 and 15 (OIR+AFLx2) or on postnatal days 13, 15 and 17. Non-injected OIR littermates (OIR) and age-matched mice housed in normoxic conditions (normoxia) were used as controls.

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Effects of Aflibercept administration at 25 mg per kg body weight in retinas of mice subjected to the oxygen-induced retinopathy protocol [P50]

Project description:We aimed at identifying the regulatory network of Aflibercept in the context of pathological neovascularization by using the oxygen-induced retinopathy mouse model as a surrogate of proliferative diabetic retinopathy Total RNA was collected from entire retinal cups dissected from 50-days old mice subjected to the oxygen-induced retinopathy protocol and subsequently injected with Aflibercept either on postnatal days 13 and 15 (OIR+AFLx2) or on postnatal days 13, 15 and 17. Non-injected OIR littermates (OIR) and age-matched mice housed in normoxic conditions (normoxia) were used as controls.

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Effects of Aflibercept administration at 25 mg per kg body weight in retinas of mice subjected to the oxygen-induced retinopathy protocol [P19]

Project description:Effects of Aflibercept administration at 25 mg per kg body weight in retinas of mice subjected to the oxygen-induced retinopathy protocol [P19]

| PRJNA566356 | ENA

Gene Expression Profile of Hyperoxic/hypoxic Retinas in Mouse Model of Oxygen-induced Retinopathy

Project description:Retinal ischemia is believed to initiate a series of events that leads to retinal neovascularization observed in several retinal diseases such as diabetetic retinopathy and retinal vein occlusion. Although some molecules such as VEGF and MCP-1 have been implicated in the process, its underlying mechanisms remain elusive. In order to identify genes associated with retinal ischemia, we performed gene expression analyses in retinas of mouse model of oxygen-induced retinopathy using DNA microarray technology.

2010-01-15 | GSE19886 | GEO

Hepatic transcriptome of rats treated with vehicle or fipronil (3 mg/kg/d per os for 14 days)

Project description:Fipronil (CAS #: 120068-37-3), a widely used insecticide, has been described as a thyroid disruptor in rat inducing a marked increase in thyroxine (T4) clearance resulting in a decrease in T4 plasma concentration. These effects seem to require the bioactivation of fipronil via its biotransformation into fipronil sulfone by cytochromes P450 (CYP). Here, we hypothesized that fipronil-induced thyroid disruption may, at least in part, result from the induction of hepatic enzymes involved in the metabolism of thyroid hormones. Thus, we used microarrays to perform a genome-wide analysis of the effects of fipronil on gene expression in rat liver. Liver gene expression was measured from female Wistar rats treated with vehicle (n = 7) or fipronil 3 mg/kg/day per os for 14 days (n = 8)

2013-08-22 | E-GEOD-39378 | biostudies-arrayexpress

RNA-seq analysis of mouse retinas from animals treated with 140mg/kg/day Vigabatrin

Project description:RNA-seq analysis of mouse retinas from animals treated with 140mg/kg/day Vigabatrin

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80 mg/kg mixed MCBA dosing (10 mg/kg indiv.) via PBFM

Project description:Mixed MCBA PBFM dosing of wild-type C57BL/6Crl mice. 80 mg/kg total bile acid dose (10 mg/kg individual MCBA). MCBAs included in the dosing included AlaCA, AspCA, GluCA, LeuCA, PheCA, SerCA, ThrCA, and TyrCA.

2023-10-21 | MSV000093171 | MassIVE

Transcription profiling of total of rat liver samples treated with 300 mg/kg/day myclobutanil, 300 mg/kg/day propiconazole, and 175 mg/kg/day triadimefon

Project description:The modes of triazole reproductive toxicity have been characterized by an observed increased in serum testosterone and reduced insemination and fertility indices. The key events involved in the disruption in testosterone homeostasis and reduced fertility remain unclear. Gene expression analysis was conducted on liver from Sprague Dawley rats dosed with myclobutanil (300 mg/kg/day), propiconazole (300 mg/kg/day), or triadimefon (175 mg/kg/day) for 72 hours. Pathway-based analysis highlighted key biological processes affected by all three triazoles in the liver including fatty acid catabolism, steroid metabolism, and xenobiotic metabolism. Within the pathways identified in the liver, specific genes involved in phase I-III metabolism and fatty acid metabolism were affected by all three triazoles. These modulated genes are part of a network of lipid and testosterone homeostasis pathways regulated by the constitutive androstane (CAR) and pregnane X (PXR) receptors. Gene expression profiles from this study indicate triazoles activate CAR and PXR; increase fatty acid catabolism and steroid metabolism in the liver; constituting a plausible series of key events contributing to the observed disruption in testosterone homeostasis. Experiment Overall Design: A total of 12 liver samples were analyzed. Three biological replicates each for the controls, 300 mg/kg/day myclobutanil, 300 mg/kg/day propiconazole, and 175 mg/kg/day triadimefon.

2008-04-08 | E-GEOD-10409 | biostudies-arrayexpress

5.0 mg/kg MeHg exposure

Project description:In this time course pregnant CD-1 (outbred) dams were exposed to MeHg as monomethylmercuric chloride intraperitoneally on 9 d.p.c. The test dose of 5.0 mg/kg MeHg was selected as a dose with an estimated 20% increased risk for encephalopathy in term fetuses, with no evidence of maternal toxicosis. Sampling intervals ranged from 1.5h to 24.0h post-exposure. All measurements were on RNA from the embryonic forebrain (prosencephalon) using contemporous control embryos as a reference. Keywords = time series Keywords = mercury Keywords = embryo Keywords = Fetal Minamata Disease Keywords: time-course

2004-03-11 | GSE1076 | GEO

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