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Second Ligand (second + ligand)

Distribution by Scientific Domains
Medical Sciences50%

Selected Abstracts

Novel Heteroleptic CuI Complexes with Tunable Emission Color for Efficient Phosphorescent Light-Emitting Diodes,

ADVANCED FUNCTIONAL MATERIALS, Issue 15 2007
Q. Zhang
Abstract A series of orange-red to red phosphorescent heteroleptic CuI complexes (the first ligand: 2,2,-biquinoline (bq), 4,4,-diphenyl-2,2,-biquinoline (dpbq) or 3,3,-methylen-4,4,-diphenyl-2,2,-biquinoline (mdpbq); the second ligand: triphenylphosphine or bis[2-(diphenylphosphino)phenyl]ether (DPEphos)) have been synthesized and fully characterized. With highly rigid bulky biquinoline-type ligands, complexes [Cu(mdpbq)(PPh3)2](BF4) and [Cu(mdpbq)(DPEphos)](BF4) emit efficiently in 20,wt,% PMMA films with photoluminescence quantum yield of 0.56 and 0.43 and emission maximum of 606,nm and 617,nm, respectively. By doping these complexes in poly(vinyl carbazole) (PVK) or N -(4-(carbazol-9-yl)phenyl)-3,6-bis(carbazol-9-yl) carbazole (TCCz), phosphorescent organic light-emitting diodes (OLEDs) were fabricated with various device structures. The complex [Cu(mdpbq)(DPEphos)](BF4) exhibits the best device performance. With the device structure of ITO/PEDOT/TCCz:[Cu(mdpbq)(DPEphos)](BF4) (15,wt,%)/TPBI/LiF/Al (III), a current efficiency up to 6.4,cd,A,1 with the Commission Internationale de L'Eclairage (CIE) coordinates of (0.61, 0.39) has been realized. To our best knowledge, this is the first report of efficient mononuclear CuI complexes with red emission. [source]

Expression Of O-Acetyl Sialic Acid On Cerebral Microcirculation In A Glycine Or Taurine Treated Diabetic Rat Model

JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000
A Noe
Expression of sialic acid is altered in Diabetes mellitus. This modification has also been involved with both vascular and neurologic diseases, and with the increase of no enzymatic glycosylation of proteins. In our opinion, the lectins were very useful with specificity for sialic acids in order to determine the level of sialic acid expression on cerebral microcirculation in a diabetic Wistar rat model with streptozotocin. In this model, the glycine (1%) and taurine (0.5%) aminoacids were placed in drinking-water by six months. At the end of this time, the animals were sacrificed, their brains surgically removed and frozen in liquid nitrogen, and the specimens cut in serial sections. Immediately, the sections were incubated with different biotin-labelled lectins specific to sialic acid using peroxidase-labelled avidin as second ligand and H2O2 chromogen. The results showed greater O-acetyl sialic acid expression in cerebral capillaries of untreated diabetic rats than in glycine-, taurine-treated diabetic rats or than in control animals. The minor sialic acid expression may be an indicator of degenerative diseases such as Alzheimer's or the vascular disease of diabetic patients and probably is related to cellular protective properties of the glycine and taurine aminoacids. These first protective characteristics that have been observed in both ischemia with cellular ATP depletion models, suggest the utilization of aminoacids glycine or taurine in diabetic patient in order to avoid the development of microinfarcts. [source]

catena -Poly[[[(iminodiacetato-,O)silver(I)]-,3 -2-aminopyrimidine-,3N1:N2:N3] monohydrate]: a one-dimensional silver(I) coordination polymer with mixed ligands

ACTA CRYSTALLOGRAPHICA SECTION C, Issue 8 2009
Di Sun
The title compound, {[Ag(C4H6NO4)(C4H5N3)]·H2O}n, was synthesized by the reaction of silver(I) nitrate with 2-aminopyrimidine and iminodiacetic acid. X-ray analysis reveals that the crystal structure contains a one-dimensional ladder-like AgI coordination polymer and that N,H...O and O,H...O hydrogen bonding results in a three-dimensional network. The AgI centre is four-coordinated by three N atoms from three different 2-aminopyrimidine ligands and one O atom from one iminodiacetate ligand. Comparison of the structural features with previous findings suggests that the existence of a second ligand plays an important role in the construction of such polymer frameworks. [source]

Emerging pharmacology and physiology of neuromedin U and the structurally related peptide neuromedin S

BRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2009
JD Mitchell
Neuromedin U (NMU) has been paired with the G-protein-coupled receptors (GPRs) NMU1 (formely designated as the orphan GPR66 or FM-3) and NMU2 (FM-4 or hTGR-1). Recently, a structurally related peptide, neuromedin S (NMS), which shares an amidated C-terminal heptapeptide motif, has been identified in both rat and human, and has been proposed as a second ligand for these receptors. Messenger RNA encoding NMU receptor subtypes shows differential expression: NMU1 is predominantly expressed in peripheral tissues, particularly the gastrointestinal tract, whereas NMU2 is abundant within the brain and spinal cord. NMU peptide parallels receptor distribution with highest expression in the gastrointestinal tract and specific structures within the brain, reflecting its major role in the regulation of energy balance. The NMU knockout mouse has an obese phenotype and, in agreement, the Arg165Trp amino acid variant of NMU-25 in humans, which is functionally inactive, co-segregated with childhood-onset obesity. Emerging physiological roles for NMU include vasoconstriction mediated predominantly via NMU1 with nociception and bone remodelling via NMU2. The NMU system has also been implicated in the pathogenesis of septic shock and cancers including bladder carcinoma and acute myeloid leukaemia. Intriguingly, NMS is more potent at NMU2 receptors in vivo where it has similar central actions in suppression of feeding and regulation of circadian rhythms to NMU. Taken together with its vascular actions, NMU may be a functional link between energy balance and the cardiovascular system and may provide a future target for therapies directed against the disorders that comprise metabolic syndrome. [source]