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A novel derivative of oligo(phenylenvinylene) (OPV), 2,5-diphenyl -1, 4-distyrylbenzene with two trans-double bonds (trans-DPDSB), is used as a blue emitting material in blue and white organic light-emitting devices (OLEDs). Blue devices with a configuration of indium-tin oxide (ITO)/N,N´-diphenyl-N,N´-bis(1-naphthyl)-(1,1´-biphenyl)-4,4´-diamine (NPB)/ trans-DPDSB / tris (8-hydroxyquinoline) aluminum (Alq3)/LiF/Al are constructed, where NPB, Alq3 and trans-DPDSB are used as hole-transporting, electron-transporting and light-emitting layers, respectively. The color of emission is changed from blue-green to pure blue when the trans-DPDSB layer is thicker. By inserting an ultrathin 5,6,11,12-tetraphenylnaphthacene (rubrene) yellow light-emitting layer between the Alq3 and trans-DPDSB layers, white OLEDs are obtained. The maximum efficiency and luminance of the blue and white devices are 1.2, 3.0 cd/A, and 1400, 7000 cd/m2, respectively.

In this paper, we describe the performance of an organic light emitting devices〔OLEDs〕 with ITO /4,4’,4“-tris{N,- （ 3-methylphenyl ） -N-phenylamino}triphenylamine (m-MTDATA) /N,N-diphenyl-N,N-bis1-naphthyl-1,1-biphenyl-4,4-diamine (NPB) /copper phthalocyanine (CuPc) / NPB / Bathocuproine(BCP) / tris-8-hydroxyquinoline Aluminum (Alq3) / LiF/ AL structure, the CuPc inserted between the two layers of NPB as a hole-consuming layer (HCL), and the BCP as a hole-blocking layer (HBL) . The EL spectrum peak is at 430 nm, indicating that the carrier recombination is confined in the NPB layer, in additional light emission originates from NPB. Compared with the luminous efficiency of the conventional diode without CuPc layer, that of the diode with HCL has been sharply increased up to 2.62 cd /A. It suggested that the CuPc and BCP exactly function as hole-consuming and hole-blocking layers, respectively, which enhance the efficiency of carrier，s recombination and confine the excitation in the EL layer.

We have fabricated an organic light-emitting devices with high efficiency and brightness utilizing thick layer of a starburst amine compound 4,4’, 4’’-tris{N,-(3-methylphenyl)-Nphenylamin} triphenylamine (m-MTDATA) as hole injection buffer layer. The brightness and the current efficiency were comparatively improved compared with those of the device without the buffer layer. The device with 10nm m-MTDATA act as buffer layer has max brightness was 18590cd/m2 at 17 V, and the highest luminous efficiency was achieved 4.30cd/A, at 7V, which is nearly three times than that of the device without it.

we designed and fabricated a white organic light-emitting device based on{[2-methyl-6-[2-(2,3,6,7-tetrahydro-1H,5H-benzo[ij]quinolizin-9yl)ethenyl]-4H-pyran-4-ylidene] propane-dinitrile}ultrathin layer and 4,4 ´ -bis(2,2 ˊ diphenylvinyl)-1,1 ˊ -biphenyl. It shows a maximum power efficiency of 1.8l m/W at 4 V (the brightness is 51 cd/m2). Its brightness reaches 8496 cd/m2 at 16 V. And the chromaticity coordinates varying from (0.42,0.34) to (0.32,0.28) with the forward bias from 4 to 16 V are well within the white region.

The lifetime of organic light-emitting devices can be influenced by the OLED material and structure, electrode material, driving mode and so on. Among all these factors, OLED driving method has been regarded as one of the most important factors, and it is well known that ac-driving mode improves the lifetime of OLED, especially pulse-driving mode with a reversed-biased voltage on OLED. In this article, a new ac-driving mode for Active-Matrix OLED is proposed on basic fabrication of two-TFT current source pixel circuit. Simulation has been done on the pixel and 1×4 matrix circuits, and simulation results have demonstrated that OLED is in reversed-biased state during recovery time. At last, a practical peripheral circuit that can provide achieve an ac-driving mode has been designed.

Neural stem cells (NSCs) reside in the anterior portion of the forebrain subventricular zone (SVZa) and generate the progenitors which will differentiate into neurons, and via a tangential migratory pathway, known as the rostral migratory stream (RMS), migrate to the olfactory bulbs (OB). Bone morphogenetic proteins (BMPs) play significant roles in neural development at different stages and locations, but their roles have not been determined in the SVZa. To explore possible roles of BMPs in SVZa NSCs, BMP4 at various concentrations were tested for their capacity to induce SVZa NSCs. The expression of BMP4 was also examined in living cells using a reportor vector, in which the BMP4 promotor was conjugated with red fluorescent protein (RFP). In the meantime, the differentiation of SVZa NSCs was dynamically monitored by using reportor vectors of the Nestin enhancer and the promoters of TH and GFAP. In the OB, high expression of BMP4 was found using both promoter activity analysis and in situ hybridization. However, low BMP4 expression was found in the RMS and only moderate expression of BMP4 was displayed in the SVZa. The results also demonstrated that low concentrations (1-5 ng/ml) of BMP4 promoted the proliferation of SVZa NSCs but high concentrations (10-100 ng/ml) of BMP4 inhibited this proliferation. BMP4 enhanced neuron commitment before 4 days but inhibited it after 4 days. As the antagonist of BMP4, Noggin almost completely blocked all these BMP4 responses. Thus, our findings indicate that BMP4 promotes the exit from the cell cycle and triggers the differentiation of neuron progenitors in the OB. BMP4 also promotes the proliferation of the committed neuron progenitors in the RMS, but in the SVZa, BMP4 may facilitate the commitment of NSCs into astrocytes.

The dentate gyrus of the hippocampus is one of few regions in the adult mammalian brain characterized by ongoing neurogenesis. It has been demonstrated that Noggin antagonizes bone morphogenetic protein-4 (BMP4) to create a niche for subventricular zone neurogenesis. We previously demonstrated that Noggin and BMP4 showed strong expression in the proliferative subgranular layer of the dentate gyrus in adult rats. To examine the action of Noggin on cell proliferation in the dentate gyrus of adult rats, we administered antisense oligodeoxynucleotide (ASODN) to Noggin by continuous infusion into the lateral ventricle of rats. Antisense-infused rats displayed significant reduction in number of bromodeoxyuridine (BrdU) labeled cells in the dentate gyrus. This indicated that endogenous Noggin activity is important for naturally occurring cell proliferation in the dentate gyrus, and perhaps neurogenesis, and is one of the many factors involved in its regulation.

Mutations in RNA-binding Fox 1 (RBFOX1) are known to be associated with neurodevelopmental disorders including epilepsy, mental retardation and autism spectrum disorder. The deletion of the Rbfox1 gene in mice has been shown to result in heightened susceptibility to seizures. However, other studies have revealed mutations or the downregulation of RBFOX1 in specimens obtained from patients with epilepsy or malformations of cortical development (MCD). Generally, the expression of RBFOX1 varies according to tissue type. In this study, we demonstrated the upregulation of RBFOX1 protein in the cortex of patients with MCD and intractable epilepsy. Electrophysiological recordings of cultured rat cortical neurons with increased Rbfox1 expression also revealed a significantly increased amplitude of action potential (AP) and Na+ current density. Some of these neurons (26.32%) even displayed spontaneous, recurrent, epileptiform discharges (SREDs). Additionally, certain Rbfox1 target transcripts associated with epilepsy, including glutamate receptor, ionotropic, N-methyl D-aspartate 1 [Grin1, also known as N-methyl-D-aspartate receptor subunit NR1 (NMDAR1)], synaptosomal-associated protein, 25 kDa (SNAP-25 or Snap25) and sodium channel, voltage gated, type VIII, alpha subunit (Scn8a, also known as Nav1.6) were identified to be upregulated in these cultured cortical neurons with an upregulated Rbfox1 expression. These data suggest that the upregulation of RBFOX1 contributes to neuronal hyperexcitation and seizures. The upregulation of NMDAR1 (Grin1), SNAP-25 (Snap25) and Scn8a may thus be involved in Rbfox1-related neuronal hyperexcitation.

In this report, an atom efficient and facile synthetic strategy for accessing multi-diketopyrrolopyrrole (DPP)-based oligomers used in solution-processed organic field effect transistors (OFETs) and organic solar cells (OSCs) has been developed. The DPP units were successfully installed onto benzene and pyrene cores via palladium-catalyzed dehydrohalogenative coupling of mono-capped DPPs with multi-bromo-benzene or -pyrene (direct arylation), affording four oligomer small molecules (SMs 1-4) containing bis-, tri-, tri-, and tetra-DPP, respectively, in high yields of 78-96%. All the designed linear or branched DPP-based oligomers exhibit broad light absorptions, narrow band-gaps (1.60-1.73 eV), deep highest occupied molecular orbital (HOMO) levels (-5.26∼-5.18 eV), and good thermal stability (Td=390-401 °C). OFETs based on SMs 1-4 showed hole mobilities of 0.0033, 0.0056, 0.0005, and 0.0026 cm2 V(-1) s(-1), respectively. OSCs based on SMs 1-4 under one sun achieved power conversion efficiencies of 3.00%, 3.71%, 2.47%, and 1.86% accordingly, along with high open-circuit voltages of 0.86-0.94 V. For OSC devices of SM 1, SM 3, and SM 4, the solvent CHCl3 was solely employed to the formation of active layers; neither high boiling point additives nor annealing post-treatment was needed. Such a simple process benefits the large-scale production of OSCs via roll to roll technology.

Focal cortical dysplasia (FCD) represents a well-recognized cause of medically intractable epilepsy. Previous studies have indicated that seizures can reduce brain pH and then eliminate seizure discharges. Acid-sensing ion channels (ASICs) are H(+)-gated cation channels that are widely expressed in the central and peripheral nervous systems. To understand the potential roles of ASIC1a in the epileptogenesis of FCD, we investigated the expression and distribution patterns of ASIC1a in surgical specimens from patients with FCD and age-matched normal cortices (CTX). Decreased ASIC1a messenger RNA (mRNA) and protein expression were detected in FCD compared with CTX. Moreover, the expression of ASIC1a was significantly lower in FCD type II than FCD type I. Immunohistochemistry results indicated that the overall immunoreactivity of the ASIC1a staining was diminished in the dysplastic cortices of FCD compared to the CTX samples. In FCD, ASIC1a immunoreactivity was mainly observed in reactive astrocytes and a minority of malformed cells, including hypertrophic neurons, dysmorphic neurons, and balloon cells. Confocal analysis demonstrated that most malformed cells expressing ASIC1a were co-labeled with neuronal rather than astrocytic markers, indicating a neuronal lineage. In conclusion, the downregulation and altered cellular distribution of ASIC1a in FCD suggest that ASIC1a may potentially contribute to the epileptogenesis of FCD.

Microgyria is associated with epilepsy and due to developmental disruption of neuronal migration. However, the role of endogenous subventricular zone-derived neural progenitors (SDNPs) in formation and hyperexcitability has not been fully elucidated. Here, we establish a neonatal cortex freeze-lesion (FL) model, which was considered as a model for focal microgyria, and simultaneously label SDNPs by CM-DiI. Morphological investigation showed that SDNPs migrated into FL and differentiated into neuronal and glia cell types, suggesting the involvement of endogenous SDNPs in the formation of FL-induced microgyria. Patch-clamp recordings in CM-DiI positive (CM-DiI(+)) pyramidal neurons within FL indicated an increase in frequency of spontaneous action potentials, while the resting membrane potential did not differ from the controls. We also found that spontaneous excitatory postsynaptic currents (EPSCs) increased in frequency but not in amplitude compared with controls. The evoked EPSCs showed a significant increase of 10-90% in rise time and decay time in the CM-DiI(+) neurons. Moreover, paired-pulse facilitation was dramatically larger in CM-DiI(+) pyramidal neurons. Western blotting data showed that AMPA and NMDA receptors were increased to some extent in the FL cortex compared with controls, and the NMDA/AMPA ratio of eEPSCs at CM-DiI(+) pyramidal neurons was significantly increased. Taken together, our findings provide novel evidence for the contribution of endogenous SDNPs in the formation and epileptogenicity of FL-induced focal microgyria.

Focal cortical dysplasias (FCDs) are increasingly recognized as important causes of medically intractable epilepsy. To understand the potential role of the interleukin 17 (IL-17) system in the epileptogenesis of FCDs, we studied the expression patterns of the IL-17 system in 15 FCD type Ia (FCDIa), 12 FCD type IIa (FCDIIa), and 12 FCD type IIb (FCDIIb) cortical lesions and compared the results with those in cerebral cortex from 10 control patients. Protein levels of IL-17, IL-17 receptor (IL-17R), and downstream factors of the IL-17 pathway (nuclear factor-κB activator 1 [NFκB; ACT1] and NFκB-p65) were markedly elevated in FCDIa, FCDIIa, and FCDIIb. Moreover, protein levels of IL-17 and IL-17R positively correlated with the frequency of seizures in FCD patients. Immunostaining indicated that IL-17 and IL-17R are highly expressed in neuronal microcolumns, dysmorphic neurons, balloon cells, astrocytes, and vascular endothelial cells. Nuclear factor-κB activator 1 and NFκB-p65 were diffusely expressed in FCDs. In addition, we detected a few IL-17-positive, CD4-positive T lymphocytes in FCDIIa and FCDIIb but not in FCDIa. Taken together, these findings suggest that the overexpression of the IL-17 system and the activation of the IL-17 signal transduction pathway may be involved in the epileptogenicity of cortical lesions in FCDs, thus representing a novel potential target for antiepileptic therapy.

Transient receptor potential vanilloid type-1 (TRPV1) is a ligand-gated nonselective cation channel that has been well characterized in peripheral pain pathway. Recent evidence from animal models of temporal lobe epilepsy (TLE) has supported the important role of TRPV1 in epileptogenesis. In this study, we investigated the expression and cellular distribution of TRPV1 in the temporal cortex (CTX) and hippocampus (HPC) from 26 patients with mesial TLE (MTLE) compared with 12 histologically normal samples. Reverse transcription-PCR and Western blotting revealed up-regulated mRNA and protein levels of TRPV1 in the MTLE group versus the control group. Immunohistochemistry data demonstrated that TRPV1 was mainly distributed in the cell bodies and dendrites of neurons. Double-labeled immunofluorescence further revealed that TRPV1 was localized on NeuN-positive neurons and GFAP-positive astrocytes, but not on HLA-positive microglia. In addition, its co-localization with glutamate and gamma-aminobutyric acid (GABA) indicated that TRPV1 was distributed on both glutamatergic and GABAergic neurons. Moreover, nerve growth factor, a sensitizing factor for TRPV1, was showed a higher expression pattern in MTLE patients. Taken together, our findings suggest that the overexpression and distribution patterns of TRPV1 might be involved in the pathogenesis and epileptogenesis of human MTLE.

The reticulon protein Nogo-A is an important regulator of neurite growth, axonal plasticity, and cell migration in the central nervous system. Previous studies have shown markedly elevated levels of Nogo-A in human temporal lobe epilepsy. In the present study, we examined the expression pattern of the Nogo-A system in cortical lesions of pediatric patients with tuberous sclerosis complex and focal cortical dysplasia type IIb. These disorders are characterized by malformations of cortical development and are frequently associated with intractable epilepsy. We found that the messenger RNA and protein levels of the Nogo-A receptor (NgR) and the downstream targets of Nogo-A, LINGO-1, TROY, and RhoA but not P75 were upregulated in the cortices of patients compared with autopsy control samples. Immunohistochemical analyses indicated that Nogo-A and NgR were strongly expressed in misshapen cells, particularly dysmorphic neurons, balloon cells, and giant cells. TROY was diffusely expressed in the malformations of cortical development. Most of the Nogo-A/NgR-positive misshapen cells were colabeled with neuronal rather than astrocytic markers. Taken together, our results suggest that the activation of Nogo-A via the NgR/LINGO-1/TROY signal transduction pathways, but not NgR/LINGO-1/P75, may be involved in the development and/or seizure activity of cortical lesions in tuberous sclerosis complex and focal cortical dysplasia type IIb.

International audience; The similarities between brain tumor stem cells and neural stem cells suggest a possible stem cell origin of tumorigenesis. Recently, cells with features of stem cells have been observed in lesions of adult and pediatric cortical dysplasia (CD). Given the evidence for a close relationship between CD and certain brain tumors, together with the finding that CD neural stem cells/progenitors are abnormally developed, we propose that CD is a possible substrate for brain tumors. The neural stem cells/progenitors in CD have accumulating abnormalities, and these abnormal stem/progenitor cells may be the initiating, transformed cells of brain tumors, when subsequently exposed to a carcinogen.

Lennox-Gastaut syndrome (LGS) is a devastating and refractory generalized epilepsy affecting children and adolescents. In this study we report the results of resective surgery in 18 patients with LGS phenotype who underwent single-lobe/lesionectomy or multilobe resection plus multiple subpial transection and/or callosotomy. After surgery, seven patients became completely seizure-free (Engel Class I) and five almost seizure-free (Engel Class II). Additional four had significant seizure control (Engel Class III), and two had no change in seizure frequency (Engel Class IV). Of the 4 patients without any lesion on brain MRI, 2 ended with Engel Class II, 1 with III and the other with IV in Engels’ classification. Mean intelligence quotient (IQ) increased from 56.1 ± 8.1 (mean ± SD) before operation to 67.4 ± 8.2 (mean ± SD) after operation, a significant improvement (P=0.001). Results also indicated that the younger the patient at surgery, or the shorter the interval between onset of seizure and resective operation, the better the intellectual outcome. Our data suggest that resective epilepsy surgery can be successful in patients with LGS phenotype as long as the EEG shows dominance of discharges in one hemisphere and corresponding ipsilateral imaging findings, even with contralateral ictal discharges.

Cortical tubers are malformations of cortical development in patients with tuberous sclerosis complex (TSC), and highly associated with pediatric intractable epilepsy. Recent evidence has shown that signaling mediated through vascular endothelial growth factor‐C (VEGF‐C) and its receptors, VEGFR‐2 and VEGFR‐3, has direct effects on both neurons and glial cells. To understand the potential role of VEGF‐C system in the pathogenesis of cortical tubers, we investigated the expression patterns of VEGF‐C signaling in cortical tubers compared with age‐matched normal control cortex (CTX). We found that VEGF‐C, VEGFR‐2 and VEGFR‐3 were clearly upregulated in tubers at both the mRNA and protein levels, compared with CTX. The in situ hybridization and immunostaining results demonstrated that VEGF‐C, VEGFR‐2 and VEGFR‐3 were highly expressed in dysplastic neurons (DNs), giant cells (GCs) and reactive astrocytes within tubers. Most DNs/GCs expressing VEGF‐C and its receptors co‐labeled with neuronal rather than astrocytic markers, suggesting a neuronal lineage. In addition, protein levels of Akt‐1, p‐Bad and ERK1/2, the important downstream factors of the VEGF‐C pathway, were significantly increased in cortical tubers, indicating involvement of VEGF‐C–dependent prosurvival signaling in cortical tubers. Taken together, our results suggest a putative role for the VEGF‐C signaling pathway in the pathogenesis of cortical tubers.

In the title mol-ecule, C(15)H(13)BrN(2)O(2), an intra-molecular O-H⋯N hydrogen bond influences the mol-ecular conformation; the two benzene rings form a dihedral angle of 13.6 (3)°. In the crystal, inter-molecular N-H⋯O hydrogen bonds link the mol-ecules into chains along the a axis and weak inter-molecular C-H⋯O hydrogen bonds further link these chains into layers parallel to the ac plane.

In the hydrazone mol-ecule of the title compound, C(15)H(12)ClN(3)O(4)·H(2)O, the two benzene rings form a dihedral angle of 3.6 (1)°. In the crystal structure, the solvent water mol-ecules are involved in the formation of inter-molecular N-H⋯O and O-H⋯N hydrogen bonds, which link the mol-ecules into double ribbons extending along the b axis. Inter-molecular π-π inter-actions between the aromatic rings [centroid-centroid distances = 3.712 (3) and 3.672 (3) Å] link these ribbons further into layers parallel to the ab plane.

Two new dioxovanadium(V) complexes, [VO 2 L 1 ] ( 1 ) and [VO 2 L 2 ] 2 ( 2 ), where L 1 and L 2 are the deprotonated forms of 4-chloro-2-[(2-piperidin-1-ylethylimino)methyl]phenol and 2-ethoxy-6-[(2-ethylaminoethylimino)methyl]phenol, respectively, have been synthesized and characterized by i.r. spectra and single crystal X-ray diffraction. Complex ( 1 ) is a mononuclear dioxovanadium complex, with the V atom five-coordinate in a distorted square pyramidal geometry. Complex ( 2 ) is a dinuclear dioxovanadium complex, with the V atom six-coordinate in an octahedral geometry. The V∙∙∙V distance is 3.096(2) A. The hydrogen bonds among the Schiff base ligands can influence the structures of the vanadium complexes. Keywords: Synthesis; vanadium complex; Schiff base; X-ray structure analysis. INTRODUCTION A wide number of studies have focused on the Schiff bases and their metal complexes in the fields of coordination chemistry, biological chemistry, and material sciences. 1–4 In the past few decades, the vanadium complexes have been found to have interesting biological activities such as normalizing the high blood glucose levels and acting as models of haloperoxidases.

In the title compound, C15H13BrN2O4·CH4O, the two benzene rings form a dihedral angle of 3.2 (2)°. An intra­molecular O—H⋯N hydrogen bond is observed. In the crystal structure, mol­ecules are linked through O—H⋯O and N—H⋯O hydrogen bonds, forming a two-dimensional network parallel to (10\overline{1}).

The molecular mechanisms and potential clinical applications of neural precursor cells have recently been the subject of intensive study. Dlx5, a homeobox transcription factor related to the distal-less gene in Drosophila, was shown to play an important role during forebrain development. The subventricular zone (SVZ) in the adult brain harbors the largest abundance of neural precursors. The anterior SVZ (SVZa) contains the most representative neural precursors in the SVZ. Further research is necessary to elucidate how Dlx5-related genes regulate the differentiation of SVZa neural precursors. Here, we employed immunohistochemistry and molecular biology techniques to study the expression of Dlx5 and related homeobox genes Er81 and Islet1 in neonatal rat brain and in in vitro cultured SVZa neural precursors. Our results show that Dlx5 and Er81 are also highly expressed in the SVZa, rostral migratory stream, and olfactory bulb. Islet1 is only expressed in the striatum. In cultured SVZa neural precursors, Dlx5 mRNA expression gradually decreased with subsequent cell passages and was completely lost by passage four. We also transfected a Dlx5 recombinant plasmid and found that Dlx5 overexpression promoted neuronal differentiation of in vitro cultured SVZa neural precursors. Taken together, our data suggest that Dlx5 plays an important role during neuronal differentiation.

International audience; Under standard culture conditions, tumor cells are exposed to 20% O(2), whereas the mean tumor oxygen levels within the tumor are much lower. We demonstrate, using low-passaged human tumor cell cultures established from glioma, that a reduction in the oxygen level in these cell cultures dramatically increases the percentage of CD133 expressing cells.

Surgery for refractory epilepsy is widely used but the efficacy of this treatment for providing a seizure-free outcome and better quality of life remains unclear. This study aimed to update current evidence and to evaluate the effects of surgery on quality of life in patients with refractory epilepsy. A systematic review and meta-analysis of the literature were conducted and selected studies included 2 groups of refractory epilepsy patients, surgical and nonsurgical. The studies were assessed using the Newcastle–Ottawa Scale. The primary outcome was the seizure-free rate. The secondary outcome was quality of life. Adverse events were also reviewed. After screening, a total of 20 studies were selected: 8 were interventional, including 2 randomized controlled trials, and 12 were observational. All of the studies comprised 1959 patients with refractory epilepsy. The seizure-free rates were significantly higher for patients who received surgery compared with the patients who did not; the combined odds ratio was 19.35 (95% CI = 12.10–30.95, P

Drug-resistance in several childhood epilepsy syndromes is common, and these patients may tolerate epilepsy surgery. In this study, the surgical outcomes of 24 pediatric patients with various intractable epilepsy syndromes and three patients with tuberous sclerosis were examined at Xinqiao hospital between 1997 and 2004. The study included nine cases of Lennox–Gastaut syndrome, two cases of Rasmussen‘s syndrome, one case of Sturge–Weber syndrome, three cases of West syndrome, three cases of tuberous sclerosis and nine cases of mesial temporal lobe epilepsy syndrome. In each case, different surgical procedures were performed according to preoperative evaluation and ECoG. At an average of 4.5 years after surgery, 14 out of 27 patients (51.9%) had an Engel Class I outcome after surgery, and an additional eight patients (29.6%) had rare seizure (Engel ClassII). Three patients showed a significant decrease in seizure frequency (Engel Class III). The mean IQ increased from 61.4 ± 12.2 to 75.0 ± 11.0, and greater IQ increase was seen in patients with shorter seizure history and drug-resistance. Temporary complications were observed in four patients and there were no deaths. In conclusion, early surgical intervention in pediatric intractable epilepsy syndromes may results in a favorable outcome in a high percentage of cases and may provides an important opportunity to prevent irreversible decline in intelligence and disability.

C16H17N3O2 ,m onoclinic, P21/n (no. 14), a =1 0.825(3) A, b =8 .916(2) A, c =1 5.310(2) A, / =1 06.291(2)°, V =1 418.3 A 3 , Z =4 , Rgt(F) =0 .0473, wRref(F 2 ) =0 .1344, T =2 98 K. Source of material Th ec ompoun dw as prepared by the condensation reaction of 3hydroxy benzaldehyde (1 mm ol, 0.122 g) and 4dimethylaminobenzohydrazide (1 mmol, 0.179 g) in anhydrous methanol (30 ml )a ta mbient temperature. Colourless blockshaped single crystals suitable for X-ray structural determination were obtained by slow evaporation of the solution for aw eek. Experimental details H(2) wa sl ocated from ad ifferenc eF ourier ma pa nd refined isotropically, with the N–H distance restrained to 0.90(1) A. The remaining Ha tom sw ere positioned geometrically and constrained to ride on their parent atoms, with C–H distances of 0.930.96 A, O–H distance of 0.82 A, and with Uiso(H) =1 .2Ueq(C) and 1.5Ueq (O1 and Cmethyl). Discussion Considerable attention has been focused on hydrazones and their medicinal applications [1-5] .T he study of the crystal structures of such compounds is of particular interest [6-8]. As ac ontinuation of our work on such compounds, we report herein the crystal structure of the title hydrazone derivative. The molecular structure of the title compound is shown in the figure. The dihedral an

C21H21N3O2, monoclinic, P21/n (no. 14), a = 10.111(2) Å, b = 6.623(2) Å, c = 26.969(2) Å, β = 98.241(2)°, V = 1787.3 Å3, Z = 4, Rgt(F) = 0.0578, wRref(F2) = 0.1544, T = 298 K.

C21H21N3O2 ,m onoclinic, P21/c (no. 14), a =5 .0165(5) A, b =1 3.148(1) A, c =2 6.705(2) A, / =9 0.198(1)°, V =1 761.4 A 3 , Z =4 , Rgt(F) =0 .0656, wRref(F 2 ) =0 .1768, T =2 98 K. Source of material Th ec ompoun dw as prepared by the condensation reaction of 2methoxy-1-naphthaldehyde (1mmol, 0.186 g) and 4dimethylaminobenzohydrazide (1mmol, 0.179 g) in anhydrous methanol (30 ml )a ta mbient temperature. Colourless blockshaped single crystals suitable for X-ray structural determination were obtained by slow evaporation of the solution for aw eek. Experimental details H(2) wa sl ocated from ad ifferenc eF ourier ma pa nd refined isotropically, with the N–H distance restrained to 0.90(1) A. The remaining Ha tom sw ere positioned geometrically and constrained to ride on their parent atoms, with C–H distances of 0.930.96 A, and with Uiso(H) =1 .2Ueq(C) and 1.5Ueq(Cmethyl).

C16H17BrN2O5, triclinic, P1 (no. 2), a = 6.934(1) A, b = 8.339(2) A, c = 14.619(2) A, 1 = 99.246(2)°, / = 91.861(2)°, . = 102.506(2)°, V = 812.5 A, Z = 2, Rgt(F) = 0.0382, wRref(F ) = 0.0907, T = 298 K.

A diketo-pyrrolo-pyrrole (DPP) oligomer containing three DPP cores (Ph4Th4(DPP)3) was synthesized via direct arylation of C-H bonds (DACH). Ph4Th4(DPP)3 has good solubility in many organic solvents, and shows a broad absorption band from the visible to near-infrared region as well as a field-effect hole mobility as high as 0.006 cm(2) V(-1) s(-1). Solution-processed bulk heterojunction organic solar cells based on blends of Ph4Th4(DPP)3 as electron donor and fullerene derivative as electron acceptor were fabricated. An optimized power conversion efficiency of 3.76% with a high open-circuit voltage of 0.85 V was achieved after finely tuning the morphology by changing the blend ratio and by adding additives. These results indicate that DACH is an effective way to produce π-conjugated oligomers for organic solar cells.

Diketopyrrolopyrrole (DPP) derivatives are an important class of high-performance pigment used in inks, paints, plastics, and organic electronics. Until now, DPP derivatives containing sophisticated aryl units at the DPP core have usually been obtained via Suzuki, Stille, or Negishi cross-coupling reactions, which require organometallic precursors. In this work, a series of DPP-based π-conjugated molecules bearing diverse aryl substituents on the thiophene- or benzene-DPPs were facilely synthesized in moderate to excellent yields through the Pd-catalyzed direct arylation of C–H bonds. The synthetic procedures feature advantages over traditional C–C cross-coupling reactions such as: (1) avoidance of the use of organometallic reagents in the starting materials leading to simpler byproducts and higher atom economy, (2) fewer synthetic steps, (3) higher yields, (4) better compatibility with chemically sensitive functional groups, and (5) simpler catalytic systems free of phosphine ligands. These advantages make the present protocol an ideal and versatile strategy for the synthesis of DPP derivatives, especially for structurally complicated DPPs that may possess chemically sensitive functionalities. The optical and electrochemical properties of the synthesized DPPs (17 compounds) were systematically investigated using UV-vis spectroscopy, steady-state fluorescence spectroscopy, and cyclic voltammetry (CV).

A graded doping technique was introduced to fabricate high brightness and high efficiency OLEDs, in which the luminescent layer consists of the mixture of NPB, Alq3 and an emitting dopant 5,6,11,12-petraphenylnaphthacene (Rubrene), where the concentration of NPB raised while the concentration of Alq 3 was declined gradually in the deposition process. This graded doping device exhibited the maximum emission of 49300cd/m 2 at 35V and the maximum efficiency of about 8cd/A at 10V, respectively, which have been improved by two times in comparison with the conventional doped devices.

In the title compound, C15H13FN2O, the dihedral angle between the benzene rings is 16.9 (2)°. The F atom and the O atom are in a syn conformation. In the crystal, molecules are linked by N—H...O hydrogen bonds to generate C(4) chains propagating along the b-axis direction.

In the title compound, C15H13N3O3, the dihedral angle between the benzene rings is 1.01 (3)° and that between the nitro group and its attached ring is 5.99 (15)°. In the crystal, molecules are linked by N—H...O hydrogen bonds generating C(4) chains along [010].

In the title compound, C(19)H(16)N(2)O(2), the benzene ring and the naphthyl ring system form a dihedral angle of 8.7 (3)° and an intra-molecular O-H⋯N hydrogen bond generates an S(6) ring. In the crystal, mol-ecules are linked by N-H⋯O hydrogen bonds, forming C(4) chains propagating in [001].

In the title compound, C(19)H(16)N(2)O(2), the benzene ring and naphthyl ring system are inclined at a dihedral angle of 16.1 (3)°. An intra-molecular O-H⋯N hydrogen bond influences the mol-ecular conformation. In the crystal, mol-ecules are linked through N-H⋯O hydrogen bonds into chains running along the a axis.

In the title compound, C(15)H(13)BrN(2)O(3), the two benzene rings form a dihedral angle of 16.9 (2)°. An intra-molecular O-H⋯N hydrogen bond affects the mol-ecular conformation. In the crystal structure, mol-ecules are linked through N-H⋯O hydrogen bonds into chains running along the a axis.

In the title compound, C(15)H(13)BrN(2)O(3), the mol-ecule adopts an E configuration about the C=N bond and the two benzene rings form a dihedral angle of 20.3 (3)°. In the mol-ecule, there are two intra-molecular hydrogen bonds, viz. O-H⋯N and N-H⋯O, involving the hy-droxy substituent, the meth-oxy O atom and the hydrazide NH group and N atom. In the crystal structure, mol-ecules are linked through N-H⋯O hydrogen bonds, forming chains propagating along [010].