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Although sensitizing traditional fluorescent dyes with thermally activated delayed fluorescence (TADF) exciplexes has been extensively studied, the device performance of solution‐processed organic light‐emitting diodes (OLEDs) still lags far behind in this regard. Herein, the novel exciplex with high up‐conversion efficiency composed of a triazatruxene‐based donor and a triazine‐based acceptor is employed as a TADF sensitizer to fluorescent dye in solution‐processed hyperfluorescent OLEDs. Benefiting from the small activation energy for triplet up‐conversion and less non‐radiative recombination of triplet excitons, the new TADF exciplex can up‐convert efficiently non‐radiative triplet excitons through reverse intersystem crossing. Besides, expeditious up‐conversion processes also shorten the residence time of triplet excitons, giving rise to significant suppression of detrimental Dexter energy transfer from the exciplex sensitizer to the dopant. By maximizing the triplet up‐conversion efficiency of exciplex sensitizers, the optimized OLEDs achieve a maximum external quantum efficiency (EQEmax) of 16.0%, which is the first report for the solution‐processed exciplex‐sensitized hyperfluorescent OLEDs with EQEmax exceeding 15%. These results validate that the up‐conversion efficiency of triplet excitons in the exciplexes strongly affects the performance of exciplex‐sensitized fluorescent devices, and the triazatruxene‐based molecules are promising donor candidates for constructing the exciplexes with high up‐conversion efficiency. [ABSTRACT FROM AUTHOR]

The hyperfluorescence has drawn great attention in achieving efficient narrowband emitting devices based on multiple resonance thermally activated delayed fluorescence (MR‐TADF) emitters. However, achieving efficient solution‐processed pure blue hyperfluorescence devices is still a challenge, due to the unbalanced charge transport and serious exciton quenching caused by that the holes are easily trapped on the high‐lying HOMO (the highest occupied molecular orbital) level of traditional diphenylamine‐decorated emitters. Here, we developed two narrowband blue organoboron emitters with low‐lying HOMO levels by decorating the MR‐TADF core with weakly electron‐donating carbazoles, which could suppress the hole trapping effect by reducing the hole traps between host and MR‐TADF emitter from deep (0.40 eV) to shallow (0.14/0.20 eV) ones for facilitating hole transport and exciton formation, as well as avoiding exciton quenching. And the large dihedral angle between the carbazole and MR‐TADF core makes the carbazole act as a steric hindrance to inhibit molecular aggregation. Accordingly, the optimized solution‐processed pure blue hyperfluorescence devices simultaneously realize record external quantum efficiency of 29.2 %, narrowband emission with a full‐width at half‐maximum of 16.6 nm, and pure blue color with CIE coordinates of (0.139, 0.189), which is the best result for the solution‐processed organic light‐emitting diodes based on MR‐TADF emitters. [ABSTRACT FROM AUTHOR]

Introduction: Reliable and valid measurement tools are crucial for clinical practice in chronic nonspecific neck pain (CNSNP). The Copenhagen Neck Functional Disability Scale (CNFDS) is a widely used scale in neck pain assessment and has its unique advantages, but it is not available for patients with CNSNP in southern China. Objective: To develop the simplified Chinese version of CNFDS (CNFDS‐SC) cross‐culturally and to investigate its measurement properties in patients with CNSNP. Design: Cross‐sectional study. Setting: Validation of neck pain measurement scale in southern China. Patients One hundred five patients with CNSNP. Interventions: Not applicable. Main Outcome Measures: Internal consistency and test‐retest reliability were evaluated using Cronbach's alpha and intraclass correlation coefficient (ICC), respectively. Construct validity and structural validity were validated by hypothesis testing and exploratory factor analysis, respectively. Internal and external responsiveness were validated. Interpretability was revealed by the standard error of measurement (SEM) and smallest detectable change (SDC). Results: Internal consistency (Cronbach's alpha = 0.77 for first test and 0.84 for retest) and test‐retest reliability (ICC = 0.95) were satisfactory. CNFDS‐SC scores showed strong correlations with the numeric rating scale (NRS), the Neck Disability Index (NDI), and the Northwick Park Neck Pain Questionnaire (NPQ) scores (r = 0.652, 0.763, and 0.719, respectively; p <.001). Factor analysis revealed a one‐factor structure of the scale. Regarding responsiveness, the standardized response mean (SRM) and the Guyatt's responsiveness index (GRI) were 1.29 and 2.12, respectively. CNFDS‐SC change scores showed good correlations with the anchoring question (r = 0.619, p <.001), NDI (r = 0.439, p =.001), and NPQ (r = 0.438 p =.001) change scores; the area under the receiver‐operating characteristic (ROC) curve was 0.89 (p <.001). The SEM and SDC were 0.93 and 2.57, respectively. No floor or ceiling effect and no missing items were observed. Conclusion: The CNFDS‐SC was demonstrated with adequate reliability, validity, responsiveness, and interpretability. The CNFDS‐SC could be an effective tool for the clinical assessment of patients with CNSNP in southern China. [ABSTRACT FROM AUTHOR]

Two boron‐, sulfur‐ and nitrogen‐doped polycyclic aromatic hydrocarbon multiple resonance thermally activated delayed fluorescence emitters with high photoluminescent quantum efficiency (88 %) and rapid reverse intersystem crossing (kRISC= 1.0×105 s−1) are designed and synthesized, enabling efficient narrow‐band blue electroluminescence at 473 nm with full width at half maximum of 29 nm and maximum external quantum efficiency of 22.0 %, which provides an avenue to expand the structure library for multiple resonance emitters and an approach to regulate their emission properties. [ABSTRACT FROM AUTHOR]

The pulsatile stress in the microcirculation may contribute to development or progression of chronic kidney disease. However, there is no prospective data confirming whether pulsatile stress in early life affect renal function in middle age. The authors performed a longitudinal analysis of 1738 participants aged 6–15 years at baseline, an ongoing Adolescent Prospective Cohort with a follow‐up of 30 years. The authors evaluated the association between pulsatile stress in childhood and adult subclinical renal damage (SRD), adjusting for related covariates. Pulsatile stress was calculated as resting heart rate × pulse pressure. Renal function was assessed with estimated glomerular filtration rate (eGFR) and urine albumin‐to‐creatinine ratio (uACR). The results showed that pulsatile stress in childhood was associated with adult SRD (Relative Risk, 1.43; p =.032), and the predictive value of combined pulse pressure and heart rate for SRD was higher than either of them alone. The high pulsatile stress in childhood increased the risk of adult SRD in males (RR, 1.92; p =.003), but this association was not found in females (RR, 0.91; p =.729). Further, the participants were categorized into four groups on the basis of pulsatile stress status in childhood and adulthood. Male patients with high pulsatile stress during childhood but normal pulsatile stress as adults still had an increased risk of SRD (RR, 2.04; 95% CI, 1.18–3.54), while female patients did not (RR, 0.96; 95% CI, 0.46–1.99). The study demonstrated that high pulsatile stress in childhood significantly increased the risk of adult SRD, especially in males. Adequate control of pulse pressure and heart rate from childhood, in the long‐term, is very important for preventing kidney damage. [ABSTRACT FROM AUTHOR]

Chromosomal rearrangements involving the mixed‐lineage leukemia (MLL1) gene are common in a unique group of acute leukemias, with more than 100 fusion partners in this malignancy alone. However, do these fusions occur or have a role in solid tumors? We performed extensive network analyses of MLL1‐fusion partners in patient datasets, revealing that multiple MLL1‐fusion partners exhibited significant interactions with the androgen‐receptor signaling pathway. Further exploration of tumor sequence data from TCGA predicts the presence of MLL1 fusions with truncated SET domain in prostate tumors. To investigate the physiological relevance of MLL1 fusions in solid tumors, we engineered a truncated version of MLL1 by fusing it with one of its known fusion partners, ZC3H13, to use as a model system. Functional characterization with cell‐based assays revealed that MLL1‐ZC3H13 fusion induced chromosomal instability, affected mitotic progression, and enhanced tumorsphere formation. The MLL1‐ZC3H13 chimera consistently increased the expression of a cancer stem cell marker (CD44); in addition, we detected potential collateral lethality between DOT1L and MLL1 fusions. Our work reveals that MLL1 fusions are likely prevalent in solid tumors and exhibit a potential pro‐tumorigenic role. This work reveals that mixed‐lineage leukemia (MLL1) fusions are likely prevalent in solid tumors and exhibit a potential pro‐tumorigenic role. Systematic analyses of the tumor‐sequencing data have identified potential MLL‐fusions in prostate tumors. Functional characterization of one such recombination using cell‐based assays revealed that this MLL1‐fusion induced chromosomal instability, affected mitotic progression, and enhanced tumorsphere formation. [ABSTRACT FROM AUTHOR]

This study investigates the trading activity in options and stock markets around informed events with extreme daily stock price movements. We find that informed agents are more likely to trade options prior to negative news and stocks ahead of positive news. We also show that optioned stocks overreact to the arrival of negative news, but react efficiently to positive news. However, the overreaction patterns are unique to the subsample of stocks with the lowest pre-event abnormal option/stock volume ratio (O/S). This finding suggests that the incremental benefit of option listing is related to the level of option trading activity, over and beyond the presence of an options market on the firm's stock. Finally, we find that the pre-event abnormal O/S is a better predictor of stock price patterns following a negative shock than is the pre-event O/S, implying that the former may contain more information about the future value of stocks than the latter. © 2014 Wiley Periodicals, Inc. Jrl Fut Mark 35:1173-1194, 2015 [ABSTRACT FROM AUTHOR]

Discovered six decades ago, transposons are known to selfishly multiply within and between chromosomes. Although they may play a creative role in building new functional parts of the genome, transposons usually cause insertional mutagenesis and/or turn nearby genes on or off. To maintain genome integrity, cells use a variety of strategies to defend against the proliferation of transposons. A class of small noncoding RNA, discovered seven years ago and called piRNA, is a new player in the war to silence transposons. piRNA is made via two biogenesis pathways: the primary processing pathway and the ping-pong amplification loop. These pathways are critically involved in transposon RNA degradation, DNA methylation, and histone modification machinery that represses transposons. In this review, we briefly introduce transposon-caused genomic instability and summarize our current understanding of the piRNA pathway, focusing on its key function in transposon silencing. © 2013 IUBMB Life, 65(9):739-747, 2013 [ABSTRACT FROM AUTHOR]

We investigate whether low-priced stocks drive long-term contrarian performance on the U.K. market. We find that contrarian performance at low, middle, and high price levels is positive. On the Fama-French risk adjusted basis, we find both low-priced and middle-priced losers have significantly positive returns. When we adjust returns by market and liquidity risk, only middle-priced losers maintain their positive returns. Our results reveal that low-priced stocks are not fully responsible for contrarian performance. Our empirical evidence is generally consistent with the overreaction hypothesis and behavioral models of value investing. [ABSTRACT FROM AUTHOR]

Bloom's syndrome (BS) and Fanconi anemia (FA) are autosomal recessive disorders characterized by cancer and chromosomal instability. BS and FA group J arise from mutations in the BLM and FANCJ genes, respectively, which encode DNA helicases. In this work, FANCJ and BLM were found to interact physically and functionally in human cells and co-localize to nuclear foci in response to replication stress. The cellular level of BLM is strongly dependent upon FANCJ, and BLM is degraded by a proteasome-mediated pathway when FANCJ is depleted. FANCJ-deficient cells display increased sister chromatid exchange and sensitivity to replication stress. Expression of a FANCJ C-terminal fragment that interacts with BLM exerted a dominant negative effect on hydroxyurea resistance by interfering with the FANCJ-BLM interaction. FANCJ and BLM synergistically unwound a DNA duplex substrate with sugar phosphate backbone discontinuity, but not an 'undamaged' duplex. Collectively, the results suggest that FANCJ catalytic activity and its effect on BLM protein stability contribute to preservation of genomic stability and a normal response to replication stress. [ABSTRACT FROM AUTHOR]

Alternate DNA structures that deviate from B-form double-stranded DNA such as G-quadruplex (G4) DNA can be formed by sequences that are widely distributed throughout the human genome. G-quadruplex secondary structures, formed by the stacking of planar quartets composed of four guanines that interact by Hoogsteen hydrogen bonding, can affect cellular DNA replication and transcription, and influence genomic stability. The unique metabolism of G-rich chromosomal regions that potentially form quadruplexes may influence a number of biological processes including immunoglobulin gene rearrangements, promoter activation and telomere maintenance. A number of human diseases are characterized by telomere defects, and it is proposed that G-quadruplex structures which form at telomere ends play an important role in telomere stability. Evidence from cellular studies and model organisms suggests that diseases with known defects in G4 DNA helicases are likely to be perturbed in telomere maintenance and cellular DNA replication. In this minireview, we discuss the connections of G-quadruplex nucleic acids to human genetic diseases and cancer based on the recent literature. [ABSTRACT FROM AUTHOR]

TRPP2, also called polycystin-2, the gene product of PKD2, is a membrane protein defective in 10–15% of cases of autosomal dominant polycystic kidney disease. Mutations in PKD2 are also associated with extrarenal disorders, such as hepatic cystogenesis and cardiovascular abnormalities. TRPP2 is a Ca-permeable nonselective cation channel present in the endoplasmic reticulum and plasma membrane, as well as in cilia of renal epithelial and embryonic nodal cells, in which it likely forms part of a flow sensor. Recent studies have identified a number of TRPP2-interacting proteins, of which many are cytoskeletal components. Work from our and other laboratories indicates that cytoskeletal partner proteins seem to play important, albeit highly complex, roles in the regulation of TRPP2 expression, localization and channel function. This minireview covers current knowledge about cytoskeletal interactions with TRPP2, and suggests that mutations in proteins of the TRPP2-cytoskeleton complex may be implicated in the pathogenesis of autosomal dominant polycystic kidney disease. [ABSTRACT FROM AUTHOR]

Polycystin-2 (PC2), encoded by PKD2, which is one of the genes whose mutations cause polycystic kidney disease, is abundantly produced in the apical domain of the syncytiotrophoblast (hST) of term human placenta. PC2, a TRP-type (TRPP2) non-selective cation channel, is present in primary cilia of renal epithelial cells, a microtubule-based ancillary structure with sensory function. The hST has abundant cytoskeletal structures, and actin filament dynamics regulate PC2 channel function in this epithelium. However, it is expected that the apical hST excludes microtubular structures. Here, we demonstrated by Western blot and immunocytochemical analyses that hST apical vesicles indeed contain microtubule structural components, including tubulin isoforms, acetylated α-tubulin, and the kinesin motor proteins KIF3A and KIF3B. PC2 and tubulin were substantially colocalized in hST vesicles. Treatment of hST vesicles with either the microtubular disrupter colchicine (15 μm) or the microtubular stabilizer paclitaxel (taxol, 15 μm) resulted in distinct patterns of microtubular re-organization and PC2 redistribution. We also observed that changes in microtubular dynamics regulate PC2 channel function. Addition of colchicine rapidly inhibited PC2 channel activity in lipid-bilayer reconstituted hST membranes. Addition of either tubulin and GTP, or taxol, however, stimulated PC2 channel activity in control hST membranes. Interestingly, we found that the kinesin motor protein KIF3A was capable of increasing PC2 channel activity in hST. We believe that the data are the first to provide a direct demonstration of a microtubular interaction with PC2 in the hST. This interaction thus plays an important regulatory role in the control of ion transport in the human placenta. [ABSTRACT FROM AUTHOR]