High brightness solution-processed OLEDs employing linear, small molecule emitters

Two novel linear oligomers that can be solution-processed to form green organic light-emitting diodes (OLEDs) are reported. Each oligomer has a donor-acceptor structure, incorporating a benzothiadiazole core with bifluorene arms attached at the 4- and 7-positions. Further electron donor behaviour is inferred from a terminal triphenylamine unit in Green 2. The resulting solution-processed OLEDs exhibited excellent performance, with a maximum luminance of 20 388 cd m-2 recorded for Green 2

An ambipolar BODIPY derivative for a white exciplex OLED and cholesteric liquid crystal laser toward multifunctional devices

A new interface engineering method is demonstrated for the preparation of an efficient white organic light-emitting diode (WOLED) by embedding an ultrathin layer of the novel ambipolar red emissive compound 4,4-difluoro-2,6-di(4-hexylthiopen-2-yl)-1,3,5,7,8-pentamethyl-4-bora-3a,4a-diaza-s-indacene (bThBODIPY) in the exciplex formation region. The compound shows a hole and electron mobility of 3.3 × 10–4 and 2 × 10–4 cm2 V–1 s–1, respectively, at electric fields higher than 5.3 × 105 V cm–1. The resulting WOLED exhibited a maximum luminance of 6579 cd m–2 with CIE 1931 color coordinates (0.39; 0.35). The bThBODIPY dye is also demonstrated to be an effective laser dye for a cholesteric liquid crystal (ChLC) laser. New construction of the ChLC laser, by which a flat capillary with an optically isotropic dye solution is sandwiched between two dye-free ChLC cells, provides photonic lasing at a wavelength well matched with that of a dye-doped planar ChLC cell

Default Risk and Equity Returns: A Comparison of the Bank-Based German and the U.S. Financial System

In this paper, we address the question whether the impact of default risk on equity returns depends on the financial system firms operate in. Using an implementation of Merton's option-pricing model for the value of equity to estimate firms' default risk, we construct a factor that measures the excess return of firms with low default risk over firms with high default risk. We then compare results from asset pricing tests for the German and the U.S. stock markets. Since Germany is the prime example of a bank-based financial system, where debt is supposedly a major instrument of corporate governance, we expect that a systematic default risk effect on equity returns should be more pronounced for German rather than U.S. firms. Our evidence suggests that a higher firm default risk systematically leads to lower returns in both capital markets. This contradicts some previous results for the U.S. by Vassalou/Xing (2004), but we show that their default risk factor looses its explanatory power if one includes a default risk factor measured as a factor mimicking portfolio. It further turns out that the composition of corporate debt affects equity returns in Germany. Firms' default risk sensitivities are attenuated the more a firm depends on bank debt financing

Reliability of clinical tests to evaluate nerve function and mechanosensitivity of the upper limb peripheral nervous system

BACKGROUND: Clinical tests to assess peripheral nerve disorders can be classified into two categories: tests for afferent/efferent nerve function such as nerve conduction (bedside neurological examination) and tests for increased mechanosensitivity (e.g. upper limb neurodynamic tests (ULNTs) and nerve palpation). Reliability reports of nerve palpation and the interpretation of neurodynamic tests are scarce. This study therefore investigated the intertester reliability of nerve palpation and ULNTs. ULNTs were interpreted based on symptom reproduction and structural differentiation. To put the reliability of these tests in perspective, a comparison with the reliability of clinical tests for nerve function was made. METHODS: Two experienced clinicians examined 31 patients with unilateral arm and/or neck pain. The examination included clinical tests for nerve function (sensory testing, reflexes and manual muscle testing (MMT)) and mechanosensitivity (ULNTs and palpation of the median, radial and ulnar nerve). Kappa statistics were calculated to evaluate intertester reliability. A meta-analysis determined an overall kappa for the domains with multiple kappa values (MMT, ULNT, palpation). We then compared the difference in reliability between the tests of mechanosensitivity and nerve function using a one-sample t-test. RESULTS: We observed moderate to substantial reliability for the tests for afferent/efferent nerve function (sensory testing: kappa = 0.53; MMT: kappa = 0.68; no kappa was calculated for reflexes due to a lack of variation). Tests to investigate mechanosensitivity demonstrated moderate reliability (ULNT: kappa = 0.45; palpation: kappa = 0.59). When compared statistically, there was no difference in reliability for tests for nerve function and mechanosensitivity (p = 0.06). CONCLUSION: This study demonstrates that clinical tests which evaluate increased nerve mechanosensitivity and afferent/efferent nerve function have comparable moderate to substantial reliability. To further investigate the clinometric properties of these tests, more studies are needed to evaluate their validity

A Large Gene Network in Immature Erythroid Cells Is Controlled by the Myeloid and B Cell Transcriptional Regulator PU.1

PU.1 is a hematopoietic transcription factor that is required for the development of myeloid and B cells. PU.1 is also expressed in erythroid progenitors, where it blocks erythroid differentiation by binding to and inhibiting the main erythroid promoting factor, GATA-1. However, other mechanisms by which PU.1 affects the fate of erythroid progenitors have not been thoroughly explored. Here, we used ChIP-Seq analysis for PU.1 and gene expression profiling in erythroid cells to show that PU.1 regulates an extensive network of genes that constitute major pathways for controlling growth and survival of immature erythroid cells. By analyzing fetal liver erythroid progenitors from mice with low PU.1 expression, we also show that the earliest erythroid committed cells are dramatically reduced in vivo. Furthermore, we find that PU.1 also regulates many of the same genes and pathways in other blood cells, leading us to propose that PU.1 is a multifaceted factor with overlapping, as well as distinct, functions in several hematopoietic lineages