Transient cognitive deficits in contextual learning.

<p>(A) Schematic of the experimental design used. (B) At 1 month post treatment, performance of radiated animals was significantly impaired compared to controls at 45 min and 24 h following training. (C) Recovery of learning and memory function was evident at 3 months post-WBRT. Data represent Mean± SEM. *p<0.0167 compared to controls.</p

Summary of the animals and behavioral tasks used for this study.

<p>Mice were behaviorally tested using the active avoidance task and Barnes maze at 1, 2, 3, 4, and 5 months post-WBRT.</p

WBRT-induced learning deficits in spatial learning are evident at 2 months.

<p>(A) Mice were subjected to fractionated WBRT and allowed to recover for 2 months, after which animals were tested in the Barnes maze. Radiated mice showed deficits in learning acquisition as measured by (B) primary errors and (C) primary latency. Performance on the Barnes maze represented as primary errors (D) and primary latency (E) over trials. No differences in memory retention (Day 10 Probe trial) (F). Data Represent Mean ± SEM. N = 9 per group. **p<0.0031; ***p<0.0001 compared to controls.</p

Changes in hippocampal vascular density after re-exposure to ambient oxygen levels.

<p>(A) Representative images of vascular density in the mouse hippocampus. Images were captured using fluorescence microscope at 10× magnification. Scale bar represents 100 µm. (B) Quantification of vascular density (length of vessels per area of tissue). Data represent Mean ± SEM. *p<0.05 vs. Control Normoxic and ^##p<0.01 vs. Radiated Normoxic. N = 5–6 animals per group/treatment.</p

Benefits of systemic hypoxia are maintained after re-exposure to normal air.

<p>A schematic of the experimental design is shown in (A). Impairments in learning, indicated by increased primary errors (B) and primary latencies (C) are observed in the radiated normoxic group. Animals that were radiated and exposed to systemic hypoxia perform similar to the controls. Data represent Mean ± SEM. ***p<0.0083 vs. Control Normoxic. N = 8–9 animals per group/treatment.</p

Working memory deficits are evident in radiated mice 4 months post-WBRT.

<p>(A) Schematic of the experimental design used. Impairments in learning occur in the radiated group as measured by: (B) primary errors and (C) primary latency over blocks of trials. Performance during individual trials is shown in (D) as primary errors and (E) as primary latency. Data represent Mean ± SEM. **p<0.00625 vs. Control. N = 9 animals per group.</p

Radiated animals are impaired in both learning and memory retention at 5 months post-treatment.

<p>A schematic of the experimental design is shown in (A). Impairments in acquisition of the task, indicated by increased primary errors (B) and primary latencies (C) are observed in the radiated group. Representation of primary errors (D) and primary latency (E) over individual trials. (F) Long-term learning retention is impaired in the radiated group. Data represent Mean ± SEM. *p<0.0031; ^#p<0.006 vs. controls. N = 8–10 animals per group.</p

Data_Sheet_1_Expression of microRNAs related to apoptosis in the aqueous humor and lens capsule of patients with glaucoma.pdf

BackgroundThe aim of this study is to investigate the expression profiles of microRNAs (miRNAs) related to apoptosis in the aqueous humor (AH) and lens capsule (LC) of patients with glaucoma.MethodsAH and LC samples were collected from patients with open-angle glaucoma and control participants who were scheduled for cataract surgery. A miRNA PCR array comprising 84 miRNAs was used to analyze the AH (glaucoma, n = 3; control, n = 3) and LC samples (glaucoma, n = 3; control, n = 4). Additionally, the AH and LC samples (glaucoma, n = 3; control, n = 4) were subjected to quantitative real-time PCR to validate the differentially expressed miRNAs determined using the PCR array. Bioinformatics analysis was performed to identify the interactions between miRNAs and diseases. Additionally, the differential expression of these miRNAs and the target gene was validated through in vitro experiments using a retinal ganglion cell (RGC) model.ResultsExpression levels of 19 and 3 miRNAs were significantly upregulated in the AH and LC samples of the glaucoma group, respectively (p 2O2-treated RGC, while the level of PTEN was recovered through co-treatment with miR-193a inhibitor or miR-222 inhibitor.ConclusionThis is the first study to investigate the differential expression of apoptosis-related miRNAs in the AH and LC of patients with glaucoma. Hsa-miR-193a-5p and hsa-miR-222-3p, which were upregulated in both AH and LC, may be considered potential biomarkers for glaucoma.</p