Investigation of glass forming ability of Al-based metallic glasses by measuring vaporization enthalpy.

The analysis of the enthalpy changes for vaporization (ΔHvap) of Al-based metallic glass (MG) can provide insight into the origin of the MG's glass forming ability (GFA). The ΔHvap of three Al-based MGs, Al84.5 ± x(Y10Ni5.5)15.5 ± x, Al85 ± x(Y8Ni5Co2)15 ± x, and Al86 ± x(Y4.5Ni6Co2La1.5)14 ± x, (hereafter referred to as AYNx, AYNCx, and AYNCLx, respectively), is analyzed by measuring their weight losses below their glass transition temperatures. The relationship between ΔHvap and aluminum concentration exhibit minimum values in the range of 83-85 at.% of Al, and the ΔHvap increases, becoming saturated at 320-350 kJ/mol, as the percentage of Al deviates from this range. The depth of the enthalpy well, referring to the bottom of the parabolic graph of ΔHvap against the Al concentration, is proportional to the viscosity of clusters showing liquid-like behavior. The amount of weight loss is proportional to the concentration of these clusters. The cluster viscosity and concentration influences the overall viscosity of the MGs, and thus determines the GFA.

Correction: Meta-Analysis of Large-Scale Toxicogenomic Data Finds Neuronal Regeneration Related Protein and Cathepsin D to Be Novel Biomarkers of Drug-Induced Toxicity.

[This corrects the article DOI: 10.1371/journal.pone.0136698.].

Meta-Analysis of Large-Scale Toxicogenomic Data Finds Neuronal Regeneration Related Protein and Cathepsin D to Be Novel Biomarkers of Drug-Induced Toxicity.

Undesirable toxicity is one of the main reasons for withdrawing drugs from the market or eliminating them as candidates in clinical trials. Although numerous studies have attempted to identify biomarkers capable of predicting pharmacotoxicity, few have attempted to discover robust biomarkers that are coherent across various species and experimental settings. To identify such biomarkers, we conducted meta-analyses of massive gene expression profiles for 6,567 in vivo rat samples and 453 compounds. After applying rigorous feature reduction procedures, our analyses identified 18 genes to be related with toxicity upon comparisons of untreated versus treated and innocuous versus toxic specimens of kidney, liver and heart tissue. We then independently validated these genes in human cell lines. In doing so, we found several of these genes to be coherently regulated in both in vivo rat specimens and in human cell lines. Specifically, mRNA expression of neuronal regeneration-related protein was robustly down-regulated in both liver and kidney cells, while mRNA expression of cathepsin D was commonly up-regulated in liver cells after exposure to toxic concentrations of chemical compounds. Use of these novel toxicity biomarkers may enhance the efficiency of screening for safe lead compounds in early-phase drug development prior to animal testing.