Anti-ECI2 (aa 1-307) polyclonal antibody

Snijders developed a family of person fit indices that asymptotically follow the standard normal distribution, when the ability parameter is estimated. So far, l z, U*, W*, ECI2 z, and ECI4 z from this family have been proposed in previous literature. One common property shared by l z, U*, and W* (also ECI2 z and ECI4 z in some specific conditions) is that they employ symmetric weight functions and thus identify spurious scores on both easy and difficult items in the same manner. However, when the purpose is to detect only the spuriously high scores on difficult items, such as cheating, guessing, and having item preknowledge, using symmetric weight functions may jeopardize the detection rates of the target aberrant response patterns. By specifying two types of asymmetric weight functions, this study proposes SHa(l)* (l = 1/ 2 or 1) and SHb(b)* (b = 2 or 3) based on Snijders's framework to specifically detect spuriously high scores on difficult items. Two simulation studies were carried out to investigate the Type I error rates and empirical power of SHa(l)* and SHb(b)*, compared with l z, U*, W*, ECI2 z, and ECI4 z. The empirical results demonstrated satisfactory performance of the proposed indices. Recommendations were also made on the choice of different person fit indices based on specific purposes.

Prostate cancer is the most common male cancer and androgen receptor (AR) is the major driver of the disease. Here we show that Enoyl-CoA delta isomerase 2 (ECI2) is a novel AR-target that promotes prostate cancer cell survival. Increased ECI2 expression predicts mortality in prostate cancer patients (p = 0.0086). ECI2 encodes for an enzyme involved in lipid metabolism, and we use multiple metabolite profiling platforms and RNA-seq to show that inhibition of ECI2 expression leads to decreased glucose utilization, accumulation of fatty acids and down-regulation of cell cycle related genes. In normal cells, decrease in fatty acid degradation is compensated by increased consumption of glucose, and here we demonstrate that prostate cancer cells are not able to respond to decreased fatty acid degradation. Instead, prostate cancer cells activate incomplete autophagy, which is followed by activation of the cell death response. Finally, we identified a clinically approved compound, perhexiline, which inhibits fatty acid degradation, and replicates the major findings for ECI2 knockdown. This work shows that prostate cancer cells require lipid degradation for survival and identifies a small molecule inhibitor with therapeutic potential.