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To utilize thermally activated delayed fluorescence (TADF) technology for future displays, it is necessary to develop host materials which harness the full potential of blue TADF emitters. However, no publication has reported such hosts yet. Although the most popular host for blue TADF, bis[2‐(diphenylphosphino)phenyl]ether oxide (DPEPO) guarantees high‐maximum external quantum efficiency (EQEmax) TADF devices, they exhibit very short operational lifetimes. In contrast, long‐lifespan blue TADF devices employing stable hosts such as 3′,5‐di(9H‐carbazol‐9‐yl)‐[1,1′‐biphenyl]‐3‐carbonitrile (mCBP‐CN) exhibit much lower EQEmax than the DPEPO‐employed devices. Here, an elaborative approach for designing host molecules is suggested to achieve simultaneously stable and efficient blue TADF devices. The approach is based on engineering the molecular geometry, ground‐ and excited‐state dipole moments of host molecules. The engineered hosts significantly enhance delayed fluorescence quantum yields of TADF emitters, as stabilizing the charge‐transfer excited states of the TADF emitters and suppressing exciton quenching, and improve the charge balance. Moreover, they exhibit both photochemical and electrochemical stabilities. The best device employing one of the engineered hosts exhibits 79% increase in EQEmax compared to the mCBP‐CN‐employed device, together with 140% and 92‐fold increases in operational lifetime compared to the respective mCBP‐CN‐ and the DPEPO‐based devices. [ABSTRACT FROM AUTHOR]

Much effort has been dedicated to increase the operational lifetime of blue phosphorescent materials in organic light‐emitting diodes (OLEDs), but the reported device lifetimes are still too short for the industrial applications. An attractive method for increasing the lifetime of a given emitter without making any chemical change is exploiting the kinetic isotope effect, where key CH bonds are deuterated. A computer model identifies that the most vulnerable molecular site in an Ir‐phenylimidazole dopant is the benzylic CH bond and predicts that deuteration may hamper the deactivation pathway involving CH/D bond cleavage notably. Experiments show that the device lifetime until the initial luminance diminishes to 70% (LT70) of a prototype phosphorescent OLED device can be doubled to 355 hours with a maximum external quantum efficiency of 25.1% at 1000 cd m−2. This is one of the best operational performances of blue phosphorescent OLEDs observed to date in a single stacked cell. [ABSTRACT FROM AUTHOR]

Although the organic light‐emitting diode (OLED) has been successfully commercialized, the development of deep‐blue OLEDs with high efficiency and long lifetime remains a challenge. Here, a novel hyperfluorescent OLED that incorporates the Pt(II) complex (PtON7‐dtb) as a phosphorescent sensitizer and a hydrocarbon‐based and multiple resonance‐based fluorophore as an emitter (TBPDP and ν‐DABNA) in the device emissive layer (EML), is proposed. Such an EML system can promote efficient energy transfer from the triplet excited states of the sensitizer to the singlet excited states of the fluorophore, thus significantly improving the efficiency and lifetime of the device. As a result, a deep‐blue hyperfluorescent OLED using a multiple resonance‐based fluorophore (ν‐DABNA) with Commission Internationale de L'Eclairage chromaticity coordinate y below 0.1 is demonstrated, which attains a narrow full width at half maximum of ≈17 nm, fourfold increased maximum current efficiency of 48.9 cd A−1, and 19‐fold improved half‐lifetime of 253.8 h at 1000 cd m−2 compared to a conventional phosphorescent OLED. The findings can lead to better understanding of the hyperfluorescent OLEDs with high performance. [ABSTRACT FROM AUTHOR]

Novel homoleptic cyclometalated Ir(III) complexes are designed to improve their emission dipole orientations in the emitting layer of blue phosphorescent organic light emitting devices. Biphenyl group is introduced into the imidazole of cyclometalated Ir(III) complexes to simultaneously achieve enhanced efficiency and operation lifetime, resulting in one of the best device performances of single‐stacked organic light emitting diodes with 91% emission dipole orientation, 26.3% maximum external quantum efficiency (maximally calculated as 41%), and 169 h lifetime at 1000 cd m−2 (LT80), color coordinate (0.17, 0.30). To elucidate the physical origin of this significant improvements, the orientational and positional distributions of the homoleptic dopants are analyzed with consideration on intermolecular interactions through atomistic modeling of the emitting layer. With the findings, the phosphorescent dopants could be designed in the future to achieve enhanced performance. [ABSTRACT FROM AUTHOR]

Irreversible chemical reactions are responsible for limited operational lifetime of organic light‐emitting devices (OLEDs). These reactions are triggered by highly reactive polaron pairs present in the emissive layer of OLEDs. Fast recombination of the polaron pairs is, therefore, crucial for slow degradation and high stability of OLED materials. Here, a study of the formation and annihilation of close polaron pairs in binary mixtures of wide bandgap hosts and a series of blue‐phosphorescent Ir(III) complex dopants, including two novel compounds, is reported. OLED devices containing doped light‐emitting layer are fabricated, and their operational lifetimes are estimated. Although inaccessible in solid films, charge recombination kinetics inside the polaron pairs is measured in liquid solutions using nanosecond laser flash photolysis. Multiscale computer simulations are applied to connect experimental results in different media and predict recombination rates in the device, with proper account taken of the inner‐ and outersphere reorganization in nonpolar materials. Predicted rates correlate with measured operational lifetimes, which demonstrates the key role of polaron pairs in the OLED degradation process. The developed methodology is useful for the rational design of novel OLED materials with higher efficiency and stability. [ABSTRACT FROM AUTHOR]

Abstract: This paper considers a replenishment problem for a single buyer who orders multiple types of items from two or more heterogeneous suppliers in order to sell to end customers. The buyer periodically orders each type of item from the suppliers according to a select inventory control policy. Processing the order, each supplier enforces the policy that an order from the buyer must meet a predetermined minimum order quantity (MOQ). Therefore, the buyer must decide how much to order from each supplier considering the current inventory level, demand forecast, and MOQ requirement. The buyer's problem is formulated as an integer programming model and an efficient implementation strategy is suggested to apply the model to real problems. Numerical experiments are performed to test the validity of the proposed model as well as the efficiency of the implementation strategy. The experimental results show that this model combined with the implementation method yields a considerable cost reduction compared to the most efficient policy currently available. [ABSTRACT FROM AUTHOR]

As wound contraction in the cutaneous layer occurs rapidly in mice, mechanical means are typically used to deliberately expose the wound to properly investigate healing by secondary intention. Previously, silicon rings and splinting models were attempted to analyze histological recovery but prevention of surrounding epidermal cell migration and subsequent closure was minimal. Here, we developed an ideal chimney wound model to evaluate epidermal regeneration in murine under hESC-EC transplantation through histological analysis encompassing the three phases of regeneration: migration, proliferation, and remodeling. Human embryonic stem cell derived endothelial cells (hESC-EC) were transplanted due to possessing a well-known therapeutic effect in angiogenesis which also enhances epidermal repair to depict the process of regeneration. Following a standard 1 mm biopsy punch, a chimney manufactured by modifying a 1.7 mL microtube was simply inserted into the excisional wound to complete the modeling process. Under this model, the excisional wound remained fully exposed for 14 days and even after 4 weeks, only a thin transparent layer of epidermal tissue covered the wound site. This approach is able to more accurately depict epidermal repair in relation to histology while also being a user-friendly and cost-effective way to mimic human recovery in rodents and evaluate epithelial repair induced by a form of therapy. [ABSTRACT FROM AUTHOR]

The effects of heteroatom substitution from a silicon atom to a germanium atom in donor-acceptor type low band gap copolymers, poly[(4,4′-bis(2-ethylhexyl)dithieno[3,2-b:2′,3′-d]silole)-2,6-diyl-alt-(2,1,3-benzothiadiazole)-4,7-diyl] (PSiBTBT) and poly[(4,4′-bis(2-ethylhexyl)dithieno[3,2-b:2′,3′-d]germole)-2,6-diyl-alt-(2,1,3-benzothiadiazole)-4,7-diyl] (PGeBTBT), are studied. The optoelectronic and charge transport properties of these polymers are investigated with a particular focus on their use for organic photovoltaic (OPV) devices in blends with phenyl-C70-butyric acid methyl ester (PC70BM). It is found that the longer C-Ge bond length, in comparison to C-Si, modifies the molecular conformation and leads to a more planar chain conformation in PGeBTBT than PSiBTBT. This increase in molecular planarity leads to enhanced crystallinity and an increased preference for a face-on backbone orientation, thus leading to higher charge carrier mobility in the diode configuration. These results provide important insight into the impact of the heavy atom substitution on the molecular packing and device performance of polymers based on the poly[2,6-(4,4-bis-(2-ethylhexyl)-4H-cyclopenta[2,1-b;3,4-b]-dithiophene)-alt-4,7-(2,1,3-benzothiadiazole) (PCPDTBT) backbone. [ABSTRACT FROM AUTHOR]

Understanding the vertical phase separation of donor and acceptor compounds in organic photovoltaics is requisite for the control of charge transport behavior and the achievement of efficient charge collection. Here, the vertically phase-separated morphologies of poly(3-hexylthiophene):[6,6]phenyl-C61-butyric acid methyl ester (P3HT:PCBM) blend films are examined with transmission electron microtomography, dynamic secondary ion mass spectroscopy, and X-ray photoelectron spectroscopy. The 3D morphologies of the processed films are analyzed and how the solvent additive causes vertical segregation is determined. The photocurrent-voltage characteristics of the vertically segregated blend films are strongly dependent on the 3D morphological organization of the donor and acceptor compounds in the photoactive layer. This dependence is correlated with asymmetric carrier transport at the buried interface and the air surface in the vertically segregated blend films. [ABSTRACT FROM AUTHOR]

Cisplatin is a chemotherapeutic agent that is widely used to treat cancers such as head and neck squamous cell carcinoma (HNSCC). Previously, we have reported that cisplatin induced an early caspase-dependent apoptosis (8 hr) in a HNSCC cell, HN4. In this study, we examined a late caspase-independent apoptosis as well as an early caspase-dependent apoptosis in cisplatin-treated HN4 cells. While z-VAD-fmk, a pan-caspase inhibitor, blocked the caspase activities and protected cells from the early apoptosis, it did not provide protection against delayed apoptosis occurring after extended exposure (16 hr) to cisplatin, suggesting that the delayed apoptotic response in the presence of z-VAD-fmk was caspase-independent. Cisplatin treatment induced reactive oxygen species (ROS) generation, loss of the mitochondrial membrane potential (MMP) and nuclear translocation of endonuclease G (EndoG). Small interfering RNA mediated-knockdown of EndoG significantly protected cells from the delayed apoptosis induced by cisplatin in the presence of z-VAD-fmk. Overexpression of Bcl-2 in HN4 cells prevented loss of MMP, nuclear translocation of EndoG and protected cells from the delayed apoptosis induced by cisplatin in the presence of z-VAD-fmk. Pretreatment with N-acetyl- [ABSTRACT FROM AUTHOR]

Objective.—The objective of this study is to determine the incidence, character, and outcome of headache in patients with unruptured intracranial aneurysms who had been treated to avoid the risk of rupture. Background.—There are a variety of clinical manifestations associated with unruptured intracranial aneurysms. Among them, chronic headache is the most common presenting and/or accompanying symptom. Methods.—Among the 137 patients with unruptured aneurysms who had been treated, we collected 81 patients excluding 30 on the basis of inclusion criteria. Twenty-six patients were lost to follow-up. We collected data by medical record review and a telephone survey. Included in the information collected was the analysis of presenting symptom, location and size of each aneurysm, location, quality, intensity and duration of headaches, associated symptoms, triggering and alleviating factors, and precipitating events. Results.—Forty-nine patients (60.5%) of 81 had chronic headaches before the diagnosis of unruptured intracranial aneurysm. Forty-four patients (89.8%) answered that their headaches were improved slightly (12 patients) or markedly (32 patients) ( P <.05). The clinical pattern of the headache worsened in only 1 patient and did not change in 4 patients. When the surgical group (40 patients) and the coil embolization group (41 patients) were compared, there was no significant difference observed in outcome ( P >.05). Conclusion.—Either by employing the technique of clipping or by coil embolization, treatment of unruptured intracranial aneurysms resulted in relief of headaches in majority of patients who had headaches pre-operatively. [ABSTRACT FROM AUTHOR]

Background.—Some patients with spontaneous intracranial hypotension (SIH) often do not demonstrate typical orthostatic headache, which is contrary to the typical SIH syndrome. They usually have an obscure and intermittent headache, regardless of their positional change. Object.—The objective of this study is to investigate the clinical course of atypical SIH that manifests with diffuse pachymeningeal enhancement, but no orthostatic headaches. Methods.—Between January 1997 and December 2005, we observed a total of 6 patients who revealed atypical presentations including nonpostural headaches and normal cerebrospinal fluid (CSF) pressure, despite the diffuse pachymeningeal enhancement seen on their MR images. For a comparison of the clinical features and the disease course, 13 other SIH patients with typical clinical manifestations were selected as a control group. Results.—Cerebrospinal fluid leakage sites were confirmed in only one patient through a variety of diagnostic tools; in contrast, definite focal CSF leakage sites were found in 12 of 13 patients with typical SIH. The 6 atypical SIH patients were treated with conservative treatment, including strict bed rest and intravenous hydration for 2 to 3 weeks. After a mean follow-up of 12 months, their headaches were gradually relieved after 2 to 3 weeks of conservative treatment only. Conclusions.—All SIHs do not necessarily show the typical clinical manifestations. The atypical finding of SIH such as nonorthostatic headache or normal CSF pressure may be the result of a normal physiologic response to the typical SIH as a compensatory reaction. Therefore, when faced with patients showing findings compatible with SIH on the brain MR images, regardless of nonpostural headache, atypical SIH should be suspected. [ABSTRACT FROM AUTHOR]

Abstract: This study demonstrates a requirement for NF-κB activation in cis-diamminedichloroplatinum (cisplatin)-induced apoptosis in human head and neck squamous cell carcinoma (HNSCC) cell lines. This conclusion was supported by the following observations: cisplatin induced IκBα degradation and NF-κB-dependent transcriptional activation prior to cell death; pyrrolidine dithiocarbamate (PDTC), a chemical inhibitor of NF-κB activation, prevented apoptosis; lactacystin, an inhibitor of IκBα degradation, also prevented apoptosis; and finally, the expression of a super-repressor mutant IκBα blocked apoptosis. The expression of tumor necrosis factor α (TNFα) was promoted by cisplatin treatment and was suppressed by PDTC treatment. In addition, a neutralizing antibody against TNFα protected cells from cisplatin-induced apoptosis. These findings suggest that NF-κB activation is required for cisplatin-induced apoptosis and TNFα may play an important role in NF-κB-mediated apoptosis in cisplatin-treated HNSCC cell lines. [Copyright &y& Elsevier]

Cisplatin is a widely used chemotherapeutic agent in head and neck squamous cell carcinoma (HNSCC). Resistance to cisplatin is a common feature of HNSCC. To identify genes that may regulate cisplatin sensitivity, we carried out a cDNA microarray analysis of gene expression in cisplatin-sensitive and cisplatin-resistant HNSCC-derived cell lines. Among genes differentially expressed by cisplatin treatment, we have confirmed the elevated expression of butyrate responsive factor 1 ( BRF1) in cisplatin-sensitive HNSCC cells and have demonstrated that the expression level of BRF1 is associated with cisplatin-sensitivity. Specific inhibition of BRF1 expression using an antisense oligodeoxynucleotide (ODN) decreased the cisplatin-sensitivity and, on the contrary, overexpression of BRF1 increased cisplatin-sensitivity in HNSCC cells. Elevated expression of BRF1 decreased the level of the human inhibitor of apoptosis protein-2 ( cIAP2) and increased the caspase-3 activity in HNSCC cells. In addition, elevated expression of BRF1 decreased the expression level of enhanced green fluorescent protein (EGFP) linked to a 3′ terminal AU-rich element (ARE) of cIAP2 mRNA. These findings demonstrate that BRF1 expression enhanced cisplatin sensitivity in HNSCC cells by reducing the levels of cIAP2 mRNA. © 2005 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Molecular programs involved in embryogenesis are frequently upregulated in oncogenic dedifferentiation and metastasis. However, their precise roles and regulatory mechanisms remain elusive. Here, we showed that CDK1 phosphorylation of TFCP2L1, a pluripotency‐associated transcription factor, orchestrated pluripotency and cell‐cycling in embryonic stem cells (ESCs) and was aberrantly activated in aggressive bladder cancers (BCs). In murine ESCs, the protein interactome and transcription targets of Tfcp2l1 indicated its involvement in cell cycle regulation. Tfcp2l1 was phosphorylated at Thr177 by Cdk1, which affected ESC cell cycle progression, pluripotency, and differentiation. The CDK1‐TFCP2L1 pathway was activated in human BC cells, stimulating their proliferation, self‐renewal, and invasion. Lack of TFCP2L1 phosphorylation impaired the tumorigenic potency of BC cells in a xenograft model. In patients with BC, high co‐expression of TFCP2L1 and CDK1 was associated with unfavorable clinical characteristics including tumor grade, lymphovascular and muscularis propria invasion, and distant metastasis and was an independent prognostic factor for cancer‐specific survival. These findings demonstrate the molecular and clinical significance of CDK1‐mediated TFCP2L1 phosphorylation in stem cell pluripotency and in the tumorigenic stemness features associated with BC progression. Synopsis: Aberrant activation of pluripotency genes is frequently observed in tumors. Thr177‐phosphorylation of TFCP2L1 by CDK1 stimulates pluripotency and cell cycling in embryonic stem cells and stemness features of bladder cancers, potentiating the tumorigenesis and aggressive behavior of bladder cancer. CDK1 phosphorylates TFCP2L1 at Thr177 in both murine embryonic stem cells (mESCs) and human bladder cancer cells.Thr177 phosphorylation of TFCP2L1 by CDK1 is essential for pluripotency and cell cycle progression of mESCs via its ability to regulate cell cycle, pluripotency and developmental gene expression.Activation of CDK1‐TFCP2L1 pathway enhances the stemness features and tumorigenesis of bladder cancer cells.Activation of the CDK1‐TFCP2L1 cascade is associated with aggressive features of bladder cancer: high tumor grade, lymphovascular invasion, muscularis‐propria invasion, metastasis to distant organs, and low patient survival rates. [ABSTRACT FROM AUTHOR]

Advances in electroluminescence demand the development of emissive molecules capable of utilizing all of the electrogenerated excitons. Here, a molecular strategy to harvest the excitons without relying on late transition metals or thermal activation is designed and evaluated. The key process deployed is an exergonic, El‐Sayed rule‐allowed reverse intersystem crossing (ES‐rISC) from the triplet n–π * transition state to the singlet π–π * transition state, followed by fluorescent decay of the latter. To demonstrate the strategy, a series of fluorescent molecules consisting of a 9,10‐diphenylanthracene core and different carbonyl n–π * units (SY compounds) is created. The compounds display a strong blue fluorescence emission with high photoluminescence quantum yields of up to 0.93. Multilayer organic electroluminescence devices containing the SY compounds exhibit maximum external quantum efficiencies greater than that obtained from a singlet‐exciton‐only control device. This improvement is due to their capacity to utilize triplet excitons for fluorescence emission. The studies demonstrate that exergonic ES‐rISC can serve as a promising pathway for creating inexpensive and tractable organic dopants for high‐efficiency electroluminescence. [ABSTRACT FROM AUTHOR]

The three‐dimensional characterization of the bulk heterojunction photoactive layer is essential for the systematic optimization of film morphologies in the development of highly efficient organic photovoltaic (OPV) devices. In article 1300612, Kilwon Cho and co‐workers report on the additiveassisted vertical phase separation of the photoactive layer in organic solar cells, which is strongly correlated with the asymmetric electrical behavior and photovoltaic parameters. [ABSTRACT FROM AUTHOR]

Background RNF213 is a major susceptibility gene for moyamoya disease (MMD), characterized by chronic progressive steno-occlusion of the intracranial arteries. However, coincidental extracranial arteriopathy is sporadically described in a few cases and in children with MMD. Methods and Results This study prospectively enrolled 63 young adults (aged 20-49 years) without a known history of systemic vascular diseases who were confirmed to have definite (bilateral, n=54) or probable (unilateral, n=9) MMD, as per typical angiographic findings. Coronary and aorta computed tomography angiography was performed to characterize extracranial arteriopathy and investigate its correlation with clinical characteristics and MMD status, including the RNF213 p.Arg4810Lys variation (c.14429G>A, rs112735431). Altogether, 11 of 63 patients (17%) had significant (>50%) stenosis in the coronary (n=6), superior mesenteric (n=2), celiac (n=2), renal (n=1), and/or internal iliac artery (n=1). One patient showed both mesenteric and iliac artery stenosis. Patients with extracranial arteriopathy were more likely to have diabetes mellitus and posterior cerebral artery involvement. Moreover, a higher prevalence of extracranial arteriopathy was observed in the presence of the RNF213 p.Arg4810Lys variant (67% in homozygotes). After controlling for diabetes mellitus and posterior cerebral artery involvement, the p.Arg4810Lys variant was independently associated with extracranial arteriopathy (additive model; P =0.035; adjusted odds ratio, 4.57; 95% CI, 1.11-27.20). Conclusions Young adults with MMD may have concomitant extracranial arteriopathy in various locations. Patients with RNF213 variants, especially the p.Arg4810Lys homozygous variant, should be screened for systemic arteriopathy.