Measurements of charge injection from indium tin oxide (ITO) into the organic semiconductor, tetraphenyl diamine doped polycarbonate (PC:TPD), were carried out. The current injected at the contact was measured as a function of the hole mobility in the organic semiconductor, which was varied from 10(-6) to 10(-3) cm (2)/V x s by adjusting the concentration of the hole transport agent, TPD, in the PC host. These experiments reveal that the current injected at the contact is proportional to the hole mobility in the bulk. As a result, the ITO/PC:TPD contact is found to limit current flow in all samples, regardless of the hole mobility in PC:TPD.

Effects of a brief orientation of lower‐class patients to the initial psychiatric interview, and a similar preparation of psychiatric residents, were compared to control patients and residents not differentially prepared. Findings relating to disposition and outcome support the authors' contention that reduction of social distance has salutary effects in making psychotherapy more accessible to disadvantaged patients. Significance of these findings for operation of a walk‐in clinic serving a lower‐class population are discussed.

Introduction and Objective The alpha globin transcription factor CP2 (TFCP2) encoded by the TFCP2 gene has been implicated in either tumor suppression or pro‐oncogenic tendencies depending on the cancer. TCFP2 has also been linked to inflammatory milieu in various diseases, making it and its regulatory targets possible prognostic markers for inflammation infiltrate levels as well as survival. This study explores the relationship between survival and predicted inflammatory features of clear cell renal cell carcinoma (ccRCC) and TFCP2‐mediated gene expression. Methods Genes which contained at least one binding site for TCFP2 in their promoter region based on ChIP‐seq data were obtained from the MSig database, and 60 genes were analyzed (including TCFP2). Kaplan‐Meier plots of overall survival in ccRCC cases in relation to TCFP2 and TCFP2‐regulated gene expression levels were generated using TCGA data, with the R2 platform “KaplanScan” algorithm creating a “high” and “low” expression cohorts (n=267,266). A step‐down Bonferroni method for multiple hypothesis correction set a significance cutoff of p<0.0033. The TIMER 2.0 platform was used to estimate immune infiltration (CD4/8+ T cells, Neutrophils, B cells, and NK cells) correlation with genes shown to be significant in terms of survival. Results From the original 60 TCFP2 and TCFP2‐mediated genes, 18 showed significant association with overall survival outcome following correction (p<0.0033), with analysis showing increased expression associated with both better (10 genes) and worse outcomes (8 genes). Immune infiltration was correlated with many of those genes, particularly in regards to CD4+ T cell and neutrophils. Weak positive correlation between CD4+ T cell infiltration and expression (r>0.30, p<0.01) was observed in 9 out of 18 genes, with one gene (EIF4G2) showing a moderate (r>0.50, p<0.001) positive correlation of r=0.554. Regarding neutrophil infiltration, 7 genes showed weak positive correlation while one gene (CDC42SE1) showed strong (r>0.70, p<0.001) positive correlation (r=0.716). For NK cells, we a saw weak negative correlation in 6 genes (‐r>|‐0.30|, p<0.01). Findings for other cells weren't significant. While TCFP2 expression itself did not show a significant association with survival, it did show a weak positive correlation with both CD4+ T cell and neutrophil infiltration and a weak negative correlation with NK levels. Conclusions Significant survival differences in the ccRCC cases were observed based on 18 different TCFP2‐regulated gene expression levels, suggesting prognostic utility. TCFP2 expression itself was not associated with a given prognosis, and further protein‐based studies may be useful to determine if this result is due to post‐transcriptional modification unaccounted for in this mRNA study. The aforementioned 18 genes also showed significant correlation with cells of the tumor immune microenvironment (TIME) such as NK, CD8+ T cells, and neutrophils, a possible route these genes may modulate survival. Previous work on hepatocellular...

Introduction and Objective Advances in our understanding of the epithelial‐mesenchymal transition (EMT), how cells change polarity and surface‐expressed proteins in acquiring a more malignant state, has aided scientists in understanding cancer progression. Using in silico tools, this study examines how EMT‐related gene expression levels are associated with survival outcomes in the rare chromophobe renal cell carcinoma (ChRCC). Methods Using dbEMT, a curated database examining EMT literature, 1184 genes were selected as “EMT‐related” for further analysis. Kaplain‐Meier Survival plots were generated based on TCGA data on all recorded ChRCC patients for each gene (n=32 in “high” and “low” groups each based on a median cut‐off), with the step‐up Bonferroni method for multiple hypothesis testing correction being used (significance being established at p<0.004). Genes identified to be statistically significant in terms of survival outcome were selected for enrichment analysis through Cytospace to examine which biological pathways might predict survival outcome. Network analysis based on physical and predicted interactions using GeneMANIA and R was done to generate a list of non‐EMT related genes which might act with those statistically significant EMT‐related genes to affect survival, with cut‐off for for significance of both network and enrichment analysis being p<0.01. DisGeNET was used to observe if the gene expression profile of ChRCC resembled any other kind of cancer. Results From the original 1184 genes, 13 showed significant change following multiple hypothesis testing correction (p<0.0038), with all showing an increased expression relating to worse outcomes. Nine distinct processes, ranging from histone modification to SMAD2/3 nuclear pathways among others, were significantly overrepresented (p<0.01) in those 13 genes. The significant EMT‐related gene signature in ChRCC mimicked the profile of mantle cell lymphoma and urothelial carcinoma. Network analysis highlighted more than 20 additional genes which EMT‐related genes could interact with to affect survival. Conclusions This study showcases a small subset of EMT‐related genes significantly overexpressed in ChRCC cases with worse prognosis. Analysis highlighted pathway dysfunction regarding microtubule cytoskeletal organization and histone modification (among others) as a possible cause of increased mortality in cases of chromophobe renal cell carcinoma. Such a preliminary in silico analysis would allow for strategically targeted wet‐lab studies.