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Normalized interventions were implemented in different cities in China to contain the outbreak of COVID-19 before December 2022. However, the differences in the intensity and timeliness of the implementations lead to differences in final size of the infections. Taking the outbreak of COVID-19 in three representative cities Xi'an, Zhengzhou and Yuzhou in January 2022, as examples, we develop a compartmental model to describe the spread of novel coronavirus and implementation of interventions to assess concretely the effectiveness of Chinese interventions and explore their impact on epidemic patterns. After applying reported human confirmed cases to verify the rationality of the model, we apply the model to speculate transmission trend and length of concealed period at the initial spread phase of the epidemic (they are estimated as 10.5, 7.8, 8.2 days, respectively), to estimate the range of basic reproduction number (2.9, 0.7, 1.6), and to define two indexes (transmission rate vt and controlled rate vc) to evaluate the overall effect of the interventions. It is shown that for Zhengzhou, vc is always more than vt with regular interventions, and Xi'an take 8 days to achieve vc > vt twice as long as Yuzhou, which can interpret the fact that the epidemic situation in Xi'an was more severe. By carrying out parameter values, it is concluded that in the early stage, strengthening the precision of close contact tracking and frequency of large-scale nucleic acid testing of non-quarantined population are the most effective on controlling the outbreaks and reducing final size. And, if the close contact tracking strategy is sufficiently implemented, at the late stage largescale nucleic acid testing of non-quarantined population is not essential. [ABSTRACT FROM AUTHOR]

Background: Pasteurella multocida (P. multocida) infection can cause a series of diseases in diferent animals and cause huge economic losses to the breeding industry. P. multocida is considered to be one of the most signifcant pathogens in rabbits. In order to elucidate the pathogenic mechanism and innate immune response of P. multocida, an infection experiment was carried out in this study. Results: Our results showed that the clinical symptoms of rabbits were severe dyspnoea and serous nasal fuid. During the course of the disease, the deaths peaked at 2days post infection (dpi) and mortality rate was 60%. The pathological changes of the lung, trachea, and thymus were observed. In particular, consolidation and abscesses appeared in lung. Histopathologic changes in rabbits showed edema, hemorrhage, and neutrophil infltration in the lung. P. multocida can rapidly replicate in a variety of tissues, and the colonization in most of the tested tissues reached the maximum at 2 dpi and then decreased at 3 dpi. The number of P. multocida in lung and thymus remained high level at 3 dpi. Toll-like receptors 2 and 4 signaling pathways were activated after P. multocida infection. The expression of Il1β, Il6, Il8, and Tnf-α was signifcantly increased. The expression of most proinfammatory cytokines peaked at 2 dpi and decreased at 3 dpi, and the expression trend of cytokines was consistent with the colonization of P. multocida in rabbit tissues. Conclusions: The P. multocida can rapidly replicate in various tissues of rabbit and cause bacteremia after infection. TLRs signaling pathways were activated after P. multocida infection, signifcantly inducing the expression of proinfammatory cytokines, which is might the main cause of respiratory infammation and septicemia. [ABSTRACT FROM AUTHOR]

Understanding the pathogenesis of nigral dopaminergic neurodegeneration is critical for developing mechanism-based treatments for Parkinson’s disease (PD). In the nigral dopaminergic neurons of postmortem human PD brains, we found that CREB, a well-recognized pro-survival transcription factor in neurons, was inactivated by dephosphorylation at Ser133. CREB dephosphorylation correlated with decreased expression of NURR1, one of its target genes crucial for dopaminergic neuron survival, confirming that CREB function was impaired in nigral dopaminergic neurons in PD. An MPTP mouse model was used to further elucidate the mechanism underlying CREB dephosphorylation. Protein phosphatase 1c (PP1γ), which dephosphorylates CREB, was constitutively associated with histone deacetylase 1 (HDAC1). HDAC1 promotes CREB Ser133 dephosphorylation via a stable interaction with PP1γ. We found that CREB interacted with the HDAC1/PP1γ complex during dopaminergic neurodegeneration. Importantly, increased CREB/HDAC1 interaction occurred in the nigral dopaminergic neurons of PD patients as demonstrated using a proximity ligation assay. Disrupting CREB/HDAC1 interaction via either overexpression of GAL4 M1, a CREB mutant, or administration of trichostatin A, a pan-HDAC inhibitor, restored the expression levels of phospho-CREB (Ser133) and NURR1, and protected nigral dopaminergic neurons in the MPTP-treated mouse brain. Collectively, our results demonstrated that HDAC1/PP1c-mediated CREB inactivation contributed to dopaminergic neuronal degeneration. Disruption of CREB/HDAC1 interaction has the potential to be a new approach for PD therapy [ABSTRACT FROM AUTHOR]

This document is an editorial published in Frontiers in Earth Science titled "Curbing carbon emissions: insight from the ecosystem evolution during ancient hyperthermal events." The editorial expresses gratitude for the contributions of international experts to the research topic, which focuses on deep-time extreme hyperthermal events and technology to mitigate carbon emissions. The editorial highlights specific studies on hyperthermal events in the Early Triassic and the Paleocene-Eocene Thermal Maximum, as well as research on natural gas exploration in diverse geological formations. The goal of the research topic is to deepen understanding of global warming and the energy transition in response to the sixth mass extinction. [Extracted from the article]

Objective: Infarction is one of the most common postoperative complications after surgical revascularization for moyamoya disease (MMD). Increased conspicuity of deep medullary veins (DMVs) on susceptibility-weighted imaging (SWI), known as "brush sign," could predict the severity of MMD. This study aimed to reveal the features of the "brush sign" in preoperative SWI and to verify its relationship to postoperative infarction. Methods: Consecutive patients with MMD who had undergone cerebral revascularization surgery were included. Routine preoperative SWI was performed. The "brush sign" was defined according to the number of the conspicuous DMVs > 5 detected on SWI. Postoperative infarctions were defined as the high-intensity signal on postoperative DWI images, with or without neurologic deficits. The modified Rankin scale (mRS) was applied to evaluate the prognosis of patients. Results: In the enrolled 100 hemispheres, 35 were presented with the "brush sign." Patients with ischemic onset manifestation and previous infarction history tended to present with the "brush sign." Multivariate analysis showed that the "brush sign" (OR 13.669; 95% CI, 1.747-106.967, p = 0.013) and decreased rCBF (OR 6.050; 95% CI, 1.052-34.799, p = 0.044) were independent risk factors of postoperative infarction. Besides, the "brush sign" showed a significant correlation with a higher mRS score at discharge (p = 0.047). Conclusion: The findings strongly suggest that the presence of the "brush sign" preoperatively can be a predictor of infarction after surgical revascularization for ischemic MMD. It may contribute to an improved surgical result through focused perioperative management based on appropriate surgical risk stratification. [ABSTRACT FROM AUTHOR]

Introduction Revascularisation surgery is an important treatment of moyamoya disease (MMD). Several general methods of revascularisation had been used: direct, indirect and combined techniques. However, there had been no reports about the criteria of recipient arteries selection in bypass surgery for MMD. Surgeons usually choose the recipient arteries by their own experiences. Their choices of the recipient arteries are various and may contribute the different outcome of patients. The purpose is to identify utility and efficacy of precision bypass guided by multimodal neuronavigation of MMD in a prospective randomised controlled trial. Method and analysis This study is a prospective randomised controlled clinical trial. This study will enrol a total of 100 eligible patients. These eligible patients will be randomised to the empirical bypass group and the multimodal neuronavigation-guided precision bypass group in a 1:1 ratio. Patient baseline characteristics and MMD characteristics will be described. In the multimodal neuronavigation-guided group, the blood velocity and blood flow of the recipient arteries will be identified. Surgical complications and outcomes at pretreatment, post-treatment, at discharge and at 3 month, 6 month, 12 month and end of trial will be analysed with CT perfusion, MRI, digital subtraction angiography, modified Rankin Scale, National Institute of Health Stroke Scale and modified Barthel Scale. This trial will determine whether multimodal neuronavigation-guided precision bypass is superior to empirical bypass in patients with MMD and identify the safety and efficacy of multimodal neuronavigation-guided precision bypass. Ethics and dissemination The study protocol and written informed consent were reviewed and approved by the Clinical Research Ethics Committee of Peking University International Hospital. Study findings will be disseminated in the printed media. The study started in August, 2018 and expected to be completed in December, 2020. Trial registration number NCT03516851; Pre-results. [ABSTRACT FROM AUTHOR]

Steroid-induced osteonecrosis of the femoral head (SONFH) is a disabling, aseptic and ischemic disease that develops following steroid therapy. The pathogenesis of SONFH is unclear, so the early diagnosis and treatment for this disease is yet to be established. The purpose of the present study was to identify potential biomarkers for SONFH. The differential expression of serum proteins from patients with SONFH and healthy volunteers was analyzed by the proteomics method. The protein samples were labeled and subjected to isoelectric focusing and two-dimensional gel electrophoresis. The resultant protein spots were matched and quantified by an imaging analysis system. The differentially-expressed protein spots were subjected to in-gel trypsin digestion followed by matrix-assisted laser desorption ionization time-of-flight mass spectrometry. Significantly lower levels of complement component 3 (C3), C4, inter-α-trypsin inhibitor heavy chain H4 and α-2-macroglobulin were found in the serum of patients with SONFH. These proteins are reported to be actively involved in intravascular coagulation, apoptosis and reactive oxygen species imbalance, indicating that multiple pathological reactions occur in SONFH and these proteins may serve as potential biomarkers for the diagnosis of SONFH. [ABSTRACT FROM AUTHOR]

We report a comparative study of the critical current density (Jc) and vortex pinning among pure and Mn doped KxFe2_ySe2 single crystals. It is found that the Jc values can be greatly improved by Mn doping and post-quenching treatment when comparing to pristine pure sample. In contrast to pure samples, an anomalous second magnetization peak (SMP) effect is observed in both 1% and 2% Mn doped samples at T = 3K for H || ab but not for H || c. Referring to Dew-Hughes and Kramer's model, we performed scaling analyses of the vortex pinning force density vs magnetic field in 1% Mn doped and quenched pristine crystals. The results show that the normal point defects are the dominant pinning sources, which probably originate from the variations of intercalated K atoms. We propose that the large nonsuperconducting K-Mn-Se inclusions may contribute to the partial normal surface pinning and give rise to the anomalous SMP effect for H || ab in Mn doped crystals. These results may facilitate further understanding of the superconductivity and vortex pinning in intercalated iron-selenides superconductors. [ABSTRACT FROM AUTHOR]

We report a new mechanism for the enhancement of porous-ZnO surface photovoltage (SPV) response to polychlorinated biphenyls (PCBs, a notorious class of persistent organic pollutants as global environmental hazard) based on copper phthalocyanine (CuPc) chemisorptive bonding on porous-ZnO. A new ZnO-CuPc composite is formed on the porous-ZnO surface due to the interaction between the surface ZnO and CuPc, with its valence band (VB) energy level being higher than that of the pristine porous-ZnO. So that the efficiency of the photogenerated-electron transfer from the composite VB to the adjacent ZnO's surface states is drastically increased due to the reduced energy gap between the transition states. As a result, the sensitivity of the PCB-orientated SPV sensor is much improved by showing amplified variation of the SPV-signals perturbed by PCBs adsorbed on the ZnO-CuPc@porous-ZnO sensitive material. [ABSTRACT FROM AUTHOR]

The band offset at CdS zinc-blende (ZB)/wurtzite (WZ) heterocrystalline interface was revisited using the first principles calculations with the local density approximation (LDA), generalized gradient approximation (GGA), and Heyd-Scuseria-Ernzerhof (HSE06) hybrid functional. It was revealed that, unlike most IV, III-V, and II-VI semiconductors, the band alignment at CdS ZB/WZ heterocrystalline interface was of type-I with straddling lineup of band edges, which was irrespective of the exchangecorrelation energy functional, the thickness of ZB and WZ segments, and the ZB/WZ interface location. The partial charge densities of VBM and CBM states were separated around two adjacent interfaces in one unit cell of heterocrystalline superlattice. This type of carrier localization was mainly attributed to the spontaneous polarization occurring in the WZ segment rather than the band offset at the interface. [ABSTRACT FROM AUTHOR]

Streptococcosis is one of the major infectious and contagious bacterial diseases for swine farm in southern China. The influence of various control measures on the outbreaks and transmission of S. suis is not currently known. In this study, in order to explore effective control and prevention measures we studied a deterministic dynamic model with stage structure for S. suis. The basic reproduction number R0 is identified and global dynamics are completely determined by R0. It shows that if R0 < 1, the disease-free equilibrium is globally stable and the disease dies out, whereas if R0 > 1, there is a unique endemic equilibrium which is globally stable and thus the disease persists in the population. The model simulations well agree with new clinical cases and the basic reproduction number of this model is about 1.1333. Some sensitivity analyses of R0 in terms of the model parameters are given. Our study demonstrates that combination of vaccination and disinfection of the environment are the useful control strategy for S. suis. [ABSTRACT FROM AUTHOR]

Cu-doped CdS thin films of variable doping levels have been deposited on indium tin oxide-coated glass substrate by simple and cost-effective ultrasonic spray pyrolysis. The influences of doping concentration and annealing treatment on the structure and photoelectrochemical properties of the films were investigated. The deposited films were characterized by XRD, SEM, and UV-Vis spectra. Moreover, the films were investigated by electrochemical and photoelectrochemical measurements with regard to splitting water for solar energy conversion. The results showed that the Cu impurity can cause a structural change and red shift of absorption edge. It was found that the photocurrent can be improved by the Cu-doping process for the unannealed films under the weak illumination. The unannealed 5 at.% Cu-doped sample obtained the maximum IPCE, which achieved about 45% at 0.3?V versus SCE potential under 420?nm wavelength photoirradiation. In addition, the p-type CdS was formed with a doping of 4 at.%~10 at.% Cu after 450°C 2 h annealed in vacuum. [ABSTRACT FROM AUTHOR]

CDK5 regulatory subunit associated protein 3 (CDK5RAP3) is a novel activator of PAK4 and processes important prometastatic function in hepatocarcinogenesis. However, it remains unclear if there are other mechanisms by which CDK5RAP3 promotes HCC metastasis. Here, we showed that in CDK5RAP3 stable knockdown SMMC-7721 HCC cells, p14ARF tumor suppressor was upregulated at protein and mRNA levels, and ectopic expression of CDK5RAP3 was found to repress the transcription of p14ARF. Using chromatin immunoprecipitation assay, we demonstrated that CDK5RAP3 bound to p14ARF promoter in vivo. Furthermore, knockdown of p14ARF in CDK5RAP3 stable knockdown HCC cells reversed the suppression of HCC cell invasiveness mediated by knockdown of CDK5RAP3. Taken together, our findings provide the new evidence that overexpression of CDK5RAP3 promotes HCC metastasis via downregulation of p14ARF. [ABSTRACT FROM AUTHOR]

A potential ultra-sensitive detection approach for hexachlorobenzene (HCB), based on the measurement of the intrinsic fluorescence of well-separated HCB molecules in ethanol, has been proposed. Owing to the strong intermolecular π–π stacking interaction of the planar aromatic rings, self-aggregated HCB shows almost no fluorescence. However, the intrinsic emission of HCB can readily be detected in ethanol due to the enhanced emission from the disaggregated HCB, which is related to the hydrogen bond formation between ethanol and HCB. By simply measuring the HCB intrinsic fluorescence, a HCB concentration a little bit higher than 10−14M (∼0.001 ppt) in ethanol can be detected; moreover, the fluorescence intensity of the HCB increases linearly with the HCB concentration ranging from 10−10to 10−7M. The approach might provide a simple, fast and efficient method for HCB quantification. [ABSTRACT FROM AUTHOR]

The proapoptotic BH3-only protein Bim is a crucial regulator of neuronal apoptosis. Previous studies have indicated the involvement of the c-Jun, FOXO1/3a, and B/C-Myb transcription factors in the regulation of Bim during neuronal apoptosis. However, the mechanism underlying the transcriptional regulation of Bim in activity deprivation-induced neuronal apoptosis has remained unclear. The present study demonstrates that early growth response 1 (Egr-1), rather than c-Jun, FOXO1/3a, or B/C-Myb, directly transactivates Bim gene expression to mediate apoptosis of rat cerebellar granule neurons. We showed that Egr-1 was sufficient and necessary for neuronal apoptosis. Suppression of Egr-1 activity using dominant-negative mutant or knockdown of Egr-1 using small interfering RNAs led to a decrease in Bim expression, whereas overexpression of Egr-1 resulted in induction of Bim. Deletion and site-directed mutagenesis of the Bim promoter revealed that Bim transcriptional activation depends primarily on a putative Egr-binding sequence between nucleotides -56 and -47 upstream of the start site.Wealso showed that Egr-1 binding to this sequence increased in response to activity deprivation in vitro and in vivo. Moreover, inhibition of Egr-1 binding to the Bim promoter, by mithramycin A and chromomycin A3, reduced the activity deprivation-induced increases in Bim promoter activity and mRNA and protein levels and protected neurons from apoptosis, further supporting the Egr-1-mediated transactivation of Bim. Additionally, Bim overcame the Egr-1 knockdown-mediated inhibition of apoptosis, whereas Bim knockdown impaired the increase in apoptosis induced by Egr-1. These findings establish Bim as an Egr-1 target gene in neurons, uncovering a novel Egr-1/Bim pathway by which activity deprivation induces neuronal apoptosis. [ABSTRACT FROM AUTHOR]

The Earth-Moon L1 libration point is proposed as a human gateway for space transportation system of the future. This paper studies indirect transfer using the perturbed stable manifold and lunar flyby to the Earth-Moon L1 libration point. Although traditional studies indicate that indirect transfer to the Earth-Moon L1 libration point does not save much fuel, this study shows that energy efficient indirect transfer using the perturbed stable manifold and lunar flyby could be constructed in an elegant way. The design process is given to construct indirect transfer to the Earth-Moon L1 libration point. Simulation results show that indirect transfer to the Earth-Moon L1 libration point saves about 420 m/s maneuver velocity compared to direct transfer, although the flight time is about 20 days longer. [ABSTRACT FROM AUTHOR]

The activator protein 1 (AP-1) transcription factor c-Jun is crucial for neuronal apoptosis. However, c-Jun dimerization partners and the regulation of these proteins in neuronal apoptosis remain unknown. Here we report that c-Jun-mediated neuronal apoptosis requires the concomitant activation of activating transcription factor-2 (ATF2) and downregulation of c-Fos. Furthermore, we have observed that c-Jun predominantly heterodimerizes with ATF2 and that the c-Jun/ATF2 complex promotes apoptosis by triggering ATF activity. Inhibition of c-Jun/ATF2 heterodimerization using dominant negative mutants, small hairpin RNAs, or decoy oligonucleotides was able to rescue neurons from apoptosis, whereas constitutively active ATF2 and c-Jun mutants were found to synergistically stimulate apoptosis. Bimolecular fluorescence complementation analysis confirmed that, in living neurons, c-Fos downregulation facilitates c-Jun/ATF2 heterodimerization. A chromatin immunoprecipitation assay also revealed that c-Fos expression prevents the binding of c-Jun/ATF2 heterodimers to conserved ATF sites. Moreover, the presence of c-Fos is able to suppress the expression of c-Jun/ATF2-mediated target genes and, therefore, apoptosis. Taken together, our findings provide evidence that potassium deprivation-induced neuronal apoptosis is mediated by concurrent upregulation of c-Jun/ATF2 heterodimerization and downregulation of c-Fos expression. This paradigm demonstrates opposing roles for ATF2 and c-Fos in c-Jun-mediated neuronal apoptosis. [ABSTRACT FROM AUTHOR]

β Amyloid protein (Aβ) and acetylcholinesterase (AChE) have been shown to be closely implicated in the pathogenesis of Alzheimer's disease. In the current study, we investigated the effects of bis(7)-tacrine, a novel dimeric AChE inhibitor, on Aβ-induced neurotoxicity in primary cortical neurons. Bis(7)-tacrine, but not other AChE inhibitors, elicited a marked reduction of both fibrillar and soluble oligomeric forms of Aβ-induced apoptosis as evidenced by chromatin condensation and DNA specific fragmentation. Both nicotinic and muscarinic receptor antagonists failed to block the effects of bis(7)-tacrine. Instead, nimodipine, a blocker of L-type voltage-dependent Ca2+ channels (VDCCs), attenuated Aβ neurotoxicity, whereas N-, P/Q- or R-type VDCCs blockers and ionotropic glutamate receptor antagonists did not. Fluorescence Ca2+ imaging assay revealed that, similar to nimodipine, bis(7)-tacrine reversed Aβ-triggered intracellular Ca2+ increase, which was mainly contributed by the extracellular Ca2+ instead of endoplasmic reticulum and mitochondria Ca2+. Concurrently, using whole cell patch-clamping technique, it was found that bis(7)-tacrine significantly reduced the augmentation of high voltage-activated inward calcium currents induced by Aβ. These results suggest that bis(7)-tacrine attenuates Aβ-induced neuronal apoptosis by regulating L-type VDCCs, offers a novel modality as to how the agent exerts neuroprotective effects. [ABSTRACT FROM AUTHOR]

GdF3:Eu3+ nanocrystals (NCs) and nanorods were synthesized by a microemulsion-mediated hydrothermalprocess. The structure, shape and particle size were characterized by means of x-ray diffraction(XRD) and transmission electron microscopy (TEM). The vacuum ultraviolet (VUV) spectrum ofGdF3:Eu3+ NCs showsthat the Gd3+ ion can absorb one VUV photon excited in the6GJ levels and relaxes through two-step energy transfer toEu3+, yielding two visible photons at room temperature. The visible quantum efficiency ofGdF3:Eu3+ NCs was calculated to be close to 170% by the peak intensity ratio of correlative transitionemission under VUV excitation at 160nm. [ABSTRACT FROM AUTHOR]

Minocycline has been shown to have remarkably neuroprotective qualities, but underlying mechanisms remain elusive. We reported here the robust neuroprotection by minocycline against glutamate-induced apoptosis through regulations of p38 and Akt pathways. Pre-treatment of cerebellar granule neurons (CGNs) with minocycline (10–100 µm) elicited a dose-dependent reduction of glutamate excitotoxicity and blocked glutamate-induced nuclear condensation and DNA fragmentations. Using patch-clamping and fluorescence Ca2+ imaging techniques, it was found that minocycline neither blocked NMDA receptors, nor reduced glutamate-caused rises in intracellular Ca2+. Instead, confirmed by immunoblots, minocyclinein vivoandin vitrowas shown to directly inhibit the activation of p38 caused by glutamate. A p38-specific inhibitor, SB203580, also attenuated glutamate excitotoxicity. Furthermore, the neuroprotective effects of minocycline were blocked by phosphatidylinositol 3-kinase (PI3-K) inhibitors LY294002 and wortmannin, while pharmacologic inhibition of glycogen synthase kinase 3β (GSK3β) attenuated glutamate-induced apoptosis. In addition, immunoblots revealed that minocycline reversed the suppression of phosphorylated Akt and GSK3β caused by glutamate, as were abolished by PI3-K inhibitors. These results demonstrate that minocycline prevents glutamate-induced apoptosis in CGNs by directly inhibiting p38 activity and maintaining the activation of PI3-K/Akt pathway, which offers a novel modality as to how the drug exerts protective effects. [ABSTRACT FROM AUTHOR]

Presents information on a study that compared the sociocultural and psychological adjustment of business expatriates from mainland China when assigned to Hong Kong, China, with their Western counterparts. Research methods; Result and discussion; Implication of the research findings for future studies.

Chinese mainland business expatriates assigned to Hong Kong were surveyed assessing their socio-cultural and psychological adjustment. The investigation explored the association of a variety of personal characteristics with adjustment to work and life in the territory. The main results of the study showed that expatriates from the neighbouring Guangdong Province, male expatriates, younger expatriates and expatriates who were accompanied by their spouses were better adjusted in Hong Kong than others. On the other hand, expatriates recruited directly from universities were less well adjusted than those hired from other sources. Implications of these findings are drawn and future avenues for improving and extending this kind of exploratory research are discussed. [ABSTRACT FROM AUTHOR]

Business expatriates from the Chinese mainland assigned to Hong Kong responded to a questionnaire regarding availability and usage of corporate career development activities. It was found that corporate development activities had a very low availability, indicating little interest on the part of the Chinese parent organizations to assist in the development of their expatriates' careers. Comparing these findings with western expatriates in the territory, the Chinese expatriates were at a clear disadvantage. Nevertheless, those career development activities that were made available by the Chinese assigning organizations were well used. [ABSTRACT FROM AUTHOR]

Efficient white organic light-emitting diodes based on copper complex, [Cu(bis[2-(diphenylphosphino)phenyl]ether)(6,7-dicyanodipyrido[2,2-d:2′,3′-f]quinoxaline)]BF4 [Cu(I) complex], in which the white emission composed of yellow emission from Cu(I) complex doped 4,4′-N,N′-dicarbazole-biphenyl (CBP) layer and blue emission from N,N′-diphenyl-N,N′-bis(1-naphthyl)-(1,1′-benzidine)-4,4′-diamine layer, were fabricated. A thin 2-(4-biphenylyl)-5-(4-tert-butyl-phenyl)-1,3,4-oxadiazole (Bu-PBD) layer sandwiched between the two emission layers acts as a chromaticity-tuning layer. The white device with 10 nm, 2 wt % Cu(I) complex doped CBP layer and 2 nm Bu-PBD layer shows CIE coordinates of (0.33,0.36) at applied bias of 10 V, a maximum luminance of 2466 cd/m2, and a maximum current efficiency of 6.76 cd/A, corresponding to the power efficiency of 3.85 lm/W. The efficient white emission is attributed to the simultaneous exciton formation in both emission layer. The working mechanism of the thin Bu-PBD layer for achieving white emission was also discussed. [ABSTRACT FROM AUTHOR]

Highly efficient orange-yellow organic electroluminescent (EL) devices based on Re(CO)3Cl-dipyrido[3,2-a:2′,3′-c]phenazine (Re-DPPz) have been fabricated. By incorporating Re-DPPz into EL devices with balanced charge injection and efficient host-to-guest energy transfer, the EL performances were significantly improved comparing with previously reports based on the same complex. For EL device with 7 wt % Re-DPPz doped emissive layer, turn-on voltage of 6 V, maximum efficiency of 6.3 cd/A, and orange-yellow emission with brightness approaching 1000 cd/m2 were achieved. The mechanism responsible for the significant improvement was discussed. [ABSTRACT FROM AUTHOR]

Electroluminescent colors of organic light-emitting diodes (OLEDs) can be tuned by modulating the thickness of gadolinium (Gd) complex layer sandwiched between an electron-transporting layer (ETL) and a hole-transporting layer (HTL). The emission colors, which originate from the two interfacial exciplexes simultaneously, can be tuned from green to orange by increasing the thickness of the Gd-complex layer. The atom force microscope images have proved that there are many gaps in the thinner Gd-complex layers. Therefore, besides the exciplex formation between Gd complex and HTL, the exciplex between ETL and HTL is also formed. The results demonstrate that a simple way of color tuning can be realized by inserting a thin layer of color tuning material between HTL with lower ionization potentials and ETL with higher electron affinities. Moreover, photovoltaic device and white OLED based on the two exciplexes are also discussed. [ABSTRACT FROM AUTHOR]

We demonstrated the fabrication of Fresnel zone plates with a 75 nm minimum feature size and circular gratings with a 20 nm minimum linewidth in polymethyl methacrylate using nanoimprint lithography, and in metals by means of a lift-off technique. Observation of sharp Moiré patterns indicated the high fidelity of nanoimprint lithography in pattern duplication. Our results showed that nanoimprint lithography is a promising technology for patterning integrated optics. © 2000 American Institute of Physics. [ABSTRACT FROM AUTHOR]