Quantification of Type, Timing, and Extent of Cell Body and Nucleus Deformations Caused by the Dimensions and Hydrophilicity of Square Prism Micropillars.

Novel digital analysis strategies are developed for the quantification of changes in the cytoskeletal and nuclear morphologies of mesenchymal stem cells cultured on micropillars. Severe deformations of nucleus and distinct conformational changes of cell body ranging from extensive elongation to branching are visualized and quantified. These deformations are caused mainly by the dimensions and hydrophilicity of the micropillars.

Prooxidant activities of alpha-lipoic acid on oxidative protein damage in the aging rat heart muscle.

In the present study, we investigated whether alpha-lipoic acid (ALA) supplementation could have prooxidant or antioxidant effects on protein oxidation parameters such as protein carbonyl (PCO), nitrotyrosine (NT), advanced oxidation protein products (AOPP), and protein thiol (P-SH), as well as oxidative stress parameters such as total thiol (T-SH), non-protein thiol (Np-SH), and lipid hydroperoxide (LHP) in the heart muscle tissue of aged rats. ALA (100 mg/kg body wt/day) was administered intraperitoneally to the experimental animals for 14 days. PCO, NT, AOPP, and P-SH levels were increased, T-SH and Np-SH levels were not changed, and only LHP levels were decreased in the heart muscle tissue of aged rats with ALA supplementation.

The effects of magnesium sulfate on blood-brain barrier disruption caused by intracarotid injection of hyperosmolar mannitol in rats.

The study was performed to evaluate whether magnesium sulfate could alter the degree of disruption of the blood-brain barrier (BBB) caused by hyperosmotic mannitol. Wistar adult female rats were infused with 25% mannitol into the left internal carotid artery. Each animal received intraperitoneally a 300 mg/kg loading dose of magnesium sulfate, dissolved in 0.

Decrease in mitochondrial oxidative protein damage parameters in the streptozotocin-diabetic rat.

Background: Many authors have shown that hyperglycemia leads to an increase in oxidative protein damage in diabetes. The aim of this study was to reveal the susceptibility of mitochondria from liver, pancreas, kidney, and skeletal muscle of diabetic Sprague-Dawley rats, a model of type 1 diabetes, to oxidative protein damage.

Methods: Mitochondrial fractions were obtained by differential centrifugation.

Soluble transferrin receptor and soluble transferrin receptor-ferritin index for evaluation of the iron status in elderly patients.

We aimed to evaluate the diagnostic values of soluble transferrin receptor (sTfR) concentration, transferrin-ferritin index (soluble transferrin receptor concentration/log ferritin), ferritin levels and other related parameters in geriatric patients with anemia of chronic disease (ACD) and iron deficiency (IDA). Forty-four elderly subjects (median age 73 [63-94]) and twenty healthy subjects (median age 49 [44-56]) were enrolled into this study, divided into four groups: twenty middle aged healthy subjects (group A), fifteen elderly patients with IDA (group B), fourteen elderly patients with ACD (group C) and fifteen nonanemic geriatric subjects (group D). Hemoglobin, mean corpuscular volume, serum iron concentration and transferrin saturation levels of the patients in IDA group were found significantly lower than those in both non-anemic group and healthy subjects.