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Retinoblastoma is a rare pediatric tumor of the retina, caused by the homozygous loss of the Retinoblastoma 1 (RB1) tumor suppressor gene. Previous microarray studies have identified changes in the expression profiles of coding genes; however, our understanding of how non-coding genes change in this tumor is absent. This is an important area of research, as in many adult malignancies, non-coding genes including LNC-RNAs are used as biomarkers to predict outcome and/or relapse. To establish a complete and in-depth RNA profile, of both coding and non-coding genes, in Retinoblastoma tumors, we conducted RNA-seq from a cohort of tumors and normal retina controls. This analysis identified widespread transcriptional changes in the levels of both coding and non-coding genes. Unexpectedly, we also found rare RNA fusion products resulting from genomic alterations, specific to Retinoblastoma tumor samples. We then determined whether these gene expression changes, of both coding and non-coding genes, were also found in a completely independent Retinoblastoma cohort. Using our dataset, we then profiled the potential effects of deregulated LNC-RNAs on the expression of neighboring genes, the entire genome, and on mRNAs that contain a putative area of homology. This analysis showed that most deregulated LNC-RNAs do not act locally to change the transcriptional environment, but potentially function to modulate genes at distant sites. From this analysis, we selected a strongly down-regulated LNC-RNA in Retinoblastoma, DRAIC, and found that restoring DRAIC RNA levels significantly slowed the growth of the Y79 Retinoblastoma cell line. Collectively, our work has generated the first non-coding RNA profile of Retinoblastoma tumors and has found that these tumors show widespread transcriptional deregulation.

A series of triphenylamine‐quinoxaline donor‐acceptor (bipolar) compounds (TPA‐QH, TPA‐QMe, TPA‐QCOOH and TPA‐QNO2) with different substituents were synthesized and investigated their fluorescence properties, including stimuli‐induced fluorescence responses in solution and the solid‐state. Single crystal structural analysis revealed non‐planar molecular conformation, substituent controlled intermolecular interactions and molecular packing in the crystal lattice. TPA‐QH, TPA‐QMe, TPA‐QCOOH and TPA‐QNO2 showed tunable solid‐state emission from green to red. TPA‐QH showed strong fluorescence at 487 nm (quantum yield (Φf)=28.3 %) whereas NO2 substituted TPA‐QNO2 exhibited relatively weak fluorescence at 610 nm (Φf=4.3 %). Density functional theoretical (DFT) calculations also indicated reduction of optical bandgap with substituting electron withdrawing group. The donor‐acceptor structure with intramolecular charge transfer (ICT) resulted solvent polarity dependent fluorescence tuning. The presence of acid responsive quinoxaline group was utilized to demonstrate pH‐responsive fluorescence switching and dual state fluorescence was utilized for fabricating rewritable fluorescent platform. Thus, the present study provides a structural insight to develop dual state emissive triphenylamine–quinoxaline based bipolar materials for optoelectronic applications. [ABSTRACT FROM AUTHOR]

Retinoblastoma is a rare pediatric tumor of the retina, caused by the homozygous loss of the Retinoblastoma 1 (RB1) tumor suppressor gene. Previous microarray studies have identified changes in the expression profiles of coding genes; however, our understanding of how non-coding genes change in this tumor is absent. This is an important area of research, as in many adult malignancies, non-coding genes including LNC-RNAs are used as biomarkers to predict outcome and/or relapse. To establish a complete and in-depth RNA profile, of both coding and non-coding genes, in Retinoblastoma tumors, we conducted RNA-seq from a cohort of tumors and normal retina controls. This analysis identified widespread transcriptional changes in the levels of both coding and non-coding genes. Unexpectedly, we also found rare RNA fusion products resulting from genomic alterations, specific to Retinoblastoma tumor samples. We then determined whether these gene expression changes, of both coding and non-coding genes, were also found in a completely independent Retinoblastoma cohort. Using our dataset, we then profiled the potential effects of deregulated LNC-RNAs on the expression of neighboring genes, the entire genome, and on mRNAs that contain a putative area of homology. This analysis showed that most deregulated LNC-RNAs do not act locally to change the transcriptional environment, but potentially function to modulate genes at distant sites. From this analysis, we selected a strongly down-regulated LNC-RNA in Retinoblastoma, DRAIC, and found that restoring DRAIC RNA levels significantly slowed the growth of the Y79 Retinoblastoma cell line. Collectively, our work has generated the first non-coding RNA profile of Retinoblastoma tumors and has found that these tumors show widespread transcriptional deregulation.

Structural analysis from powder neutron and single-crystal x-ray diffraction data for a sample of the [Tl.sub.2][Mn.sub.2][O.sub.7] pyrochlore, which exhibits colossal magnetoresistance (CMR), shows no deviations from ideal stoichiometry. This analysis gives an Mn-O distance of 1.90 angstroms, which is significantly shorter than the Mn-O distances (1.94 to 2.00 angstroms) observed in phases based on LaMn[O.sub.3] perovskites that exhibit CMR. Both results in [Tl.sub.2][Mn.sub.2][O.sub.7] indicate oxidation states very close to [Mathematical Expression Omitted]. Thus, [Tl.sub.2][Mn.sub.2][O.sub.7] has neither mixed valence for a double:exchange magnetic interaction nor a Jahn-Teller cation such as [Mn.sup.3+], both of which were thought to have an important function in CMR materials. An alternate mechanism for CMR in [Tl.sub.2][Mn.sub.2][O.sub.7] based on magnetic ordering driven by superexchange and strong spin-fluctuation scattering above the Curie temperature is proposed here., The strong correlation between magnetic moment and electrical resistance and the resulting large magnetoresistance near room temperature in lanthanum manganese oxides ([La.sub.1-x][M.sub.x]Mn[O.sub.3], where M = Ca, Sr, or Ba) is [...]

Perilipin A is the most abundant lipid droplet-associated protein in adipocytes and serves important functions in regulating triacylglycerol levels by reducing rates of basal lipolysis and facilitating hormonally stimulated lipolysis. We have previously shown that the central region of perilipin A targets and anchors it to lipid droplets, at least in part via three moderately hydrophobic sequences that embed the protein into the hydrophobic core of the droplet. The current study examines the roles of the amino and carboxyl termini of perilipin A in facilitating triacylglycerol storage. Amino- and carboxyl-terminal truncation mutations of mouse perilipin A were stably expressed in 3T3-L1 preadipocytes, which lack perilipins. Triacylglycerol content of the cells was quantified as a measure of perilipin function and was compared with that of cells expressing full-length perilipin A or control cells lacking perilipins. The aminoterminal sequence between amino acids 122 and 222, including four 10-11-amino acid sequences predicted to form amphipathic β-strands and a consensus site for cAMP-dependent protein kinase, and the carboxyl terminus of 112 amino acids that is unique to perilipin A were critical to facilitate triacylglycerol storage. The precocious expression of full-length perilipin A in 3T3-L1 preadipocytes aided more rapid storage of triacylglycerol during adipose differentiation. By contrast, the expression of highly truncated amino- or carboxylterminal mutations of perilipin failed to serve a dominant negative function in lowering triacylglycerol storage during adipose differentiation. We conclude that the amino and carboxyl termini are critical to the function of perilipin A in facilitating triacylglycerol storage. [ABSTRACT FROM AUTHOR]