A divalent heteroleptic lanthanoid fluoride complex stabilised by the tetraphenylcyclopentadienyl ligand, arising from C-F activation of pentafluorobenzene.

The divalent heteroleptic lanthanoid fluoride complex, [Yb(C5Ph4H)(µ-F)(thf)2]2, as well as [Yb(C5Ph4H)2(thf)] and [Yb(C5Ph4H)(C6F5)(thf)2] were obtained from reactions of ytterbium metal with Hg(C6F5)2 and tetraphenylcyclopentadiene under different conditions, and C-F activation of C6F5H by Yb metal was observed.

[15]crown-5: an unsymmetrical bifacial hydrogen-bond acceptor in crystal engineering.

Reaction of [15]crown-5 with erbium nitrate and a range of nickel salts results in the formation of the hydrogen-bonded chain species [Er(NO3)3(H2O)3]. [15]crown-5 H2O (3), [Ni(H2O)6]Br2 [15]crown-5 2H2O (4), [Ni(H2O)6](ClO4)2 x [15]crown-5 2H2O (5), [Ni(H2O)6](NO3)2 [15]crown-5 2H2O (6) and [[Ni(H2O)4]2(muCl)2]Cl2 [15]crown-5 (7). Complexes 3-5 exhibit low symmetry structures with 2-4 unique crown ether molecules, whereas 6 and 7 are more symmetrical. The factors contributing to this behaviour are discussed within the wider context of [15]crown-5 structures in the Cambridge Structural Database.

Syntheses, crystal structures, magnetic properties, and EPR spectra of tetranuclear copper(II) complexes featuring pairs of "roof-shaped" Cu2X2 dimers with hydroxide, methoxide, and azide bridges.

Hydroxo- and methoxo-bridged tetranuclear copper(II) complexes of the tetramacrocyclic ligand 1,2,4,5-tetrakis(1,4,7-triazacyclonon-1-ylmethyl)benzene (Ldur), have been prepared from [Cu4Ldur(H2O)8](ClO4)8.9H2O (1). Addition of base to an aqueous solution of 1 gave [Cu4Ldur(mu2-OH)4](ClO4)4 (2). Diffusion of MeOH into a DMF solution of 2 produces [Cu4Ldur(mu2-OMe)4](ClO4)4.HClO4.2/3MeOH (3), a complex which hydrolyzes on exposure to moisture regenerating 2. The structurally related azido-bridged complex, [Cu4Ldur(mu2-N3)4](PF6)4.4H2O.6CH3CN (4), was produced by reaction of Ldur with 4 molar equiv of Cu(OAc)2.H2O and NaN3 in the presence of excess KPF6. Compounds 2-4 crystallize in the triclinic space group P1 (No. 2) with a = 10.248(1) A, b = 12.130(2) A, c = 14.353(2) A, alpha = 82.23(1) degrees, beta = 80.79(1) degrees, gamma = 65.71(1) degrees, and Z = 1 for 2, a = 10.2985(4) A, b = 12.1182(4) A, c = 13.9705(3) A, alpha = 89.978(2) degrees, beta = 82.038(2) degrees, gamma = 65.095(2) degrees, and Z = 1 for 3, and a = 12.059(2) A, b = 12.554(2) A, c = 14.051(2) A, alpha = 91.85(1) degrees, beta = 98.22(1) degrees, gamma = 105.62(1) degrees, and Z = 1 for 4. The complexes feature pairs of isolated dibridged copper(II) dimers with "roof-shaped" Cu2(mu2-X)2 cores (X = OH-, OMe-, N3-), as indicated by the dihedral angle between the two CuX2 planes (159 degrees for 2, 161 degrees for 3, and 153 degrees for 4). This leads to Cu.Cu distances of 2.940(4) A for 2, 2.962(1) A for 3, and 3.006(5) A for 4. Variable-temperature magnetic susceptibility measurements indicate weak antiferromagnetic coupling (J = -27 cm(-1)) for the hydroxo-bridged copper(II) centers in 2 and very strong antiferromagnetic coupling (J = -269 cm(-1)) for the methoxo-bridged copper(II) centers in 3. Pairs of copper(II) centers in 4 display the strongest ferromagnetic interaction (J = 94 cm(-1)) reported thus far for bis(mu2-1,1-azido)-bridged dicopper units. Spectral measurements on a neat powdered sample of 4 at 33.9 GHz or 90 Ghz confirm the spin-triplet ground state for the azido-bridged copper(II) pairs.

Protonation studies of reduced ruthenium(II) complexes with polypyridyl ligands.

The pKa values associated with protonation of the one-electron reduced forms of series of [L'2Ru(II)L]2+ complexes [L' = bidentate polypyridyl ligand; L = bidentate polypyridyl ligand with additional uncoordinated N atoms in the aromatic ring system: e.g., dpp = 2,3-bis(2-pyridyl)pyrazine, bpz = 2,2'-bipyrazine] were assessed using pulse radiolysis techniques by the measurement of spectral variations as a function of pH. A linear correlation was observed between pKa and E (RuL'2L2+/+) for complexes in which the protonatable ligand was at the same time the site of reduction. In complexes where one or more of the nonprotonatable ligands (L') had very low pi* energy levels [e.g. (CF3)4bpy], reduction occurs on a nonprotonatable ligand and a dramatic decrease in the pKa values was observed for the reduced species. In complexes where the energies of the protonatable and nonprotonatable ligands were comparable, the protonation behavior was consistent with some orbital mixing/ delocalization of the electronic charge.

The biologic activity of mast cell granules. VIII. In vivo and in vitro characterization of mast cell granule-derived inflammatory factors involved in rat late-phase reactions.

Intradermal injections of isolated mast cell granules (MCGs), as well as solubilized high-molecular-weight (HMW) (greater than 10,000 daltons) and low-molecular-weight (LMW) (10,000 greater than MW greater than 500 daltons) fractionated granule constituents, can produce inflammatory responses termed late-phase reactions (LPRs). The identity and mechanism of action of various inflammatory factor(s) contained within these fractions is incompletely established. Since rat LPRs are neutrophil-dependent responses, we analyzed the inherent neutrophil chemoattractant potential of HMW and LMW granule fractions using a 48-well microchemotaxis chamber. Although both HMW and LMW fractions attracted rat neutrophils, the LMW fraction was less active at equivalent protein concentrations. Checkerboard analysis demonstrated that the HMW fraction enhanced random migration of neutrophils, indicating that the HMW fraction contains factors that are primarily chemokinetic. To analyze further the HMW fraction, solubilized MCGs were sequentially fractionated with XM300 (MW greater than 300,000 daltons), and YM100 (300,000 greater than MW greater than 100,000 daltons), XM50 (100,000 greater than MW greater than 50,000 daltons), and YM10 (50,000 greater than MW greater than 10,000 daltons) ultrafiltration membranes. This process revealed that most in vivo inflammation-provoking activity as well as the in vitro chemoattractant activity resided in the XM300 and YM100 retentate fractions. Two of the major constituents of the HMW fraction, heparin and chymase, were evaluated for their contribution to the chemoattraction. Purified MCG heparin did not evoke neutrophil migratory responses in vitro or in vivo. Sepharose 4B chromatography of solubilized MCG demonstrated a peak of inflammation-provoking activity beginning at the void volume and tapering off near the 400,000 MW range. This in vivo activity was clearly separable from the chymase activity and represents the HMW inflammatory factors. These results demonstrate that both HMW and LMW granule fractions contain inflammatory activities capable of producing LPR in vivo and suggest that enhancement of neutrophil migration at sites of mast cell degranulation is one mechanism of action.

IgE antibody mediated inflammation of rat lung: histologic and bronchoalveolar lavage assessment.

Pulmonary antigen challenge in sensitized individuals elicits immediate and late phase responses (LPR). While mast cells and tissue inflammation are thought to be vital to the development of the LPR, the precise pathogenesis of these responses remains under investigation. Using the Sprague-Dawley rat as a model to study cutaneous LPR, we have previously demonstrated that rat cutaneous LPR are mast cell-dependent and are histologically characterized by early (1-8 h) neutrophil-rich and late (8-24 h) mononuclear cell-rich infiltrates. To compare and contrast this cutaneous response with IgE-dependent pulmonary inflammatory responses, we performed bronchoalveolar lavage (BAL) analyses of pulmonary inflammation following specific antigen challenge in actively immunized [IgE anti-ovalbumin (OA) antibody] and BAL and histologic analyses in passively sensitized [mouse hybridoma anti-dinitrophenyl (DNP) IgE antibody] rats. Following direct insufflation of OA into the trachea, actively sensitized animals demonstrated an increased number of polymorphonuclear leukocytes (PMNs) at 4 h in BAL fluid. These cell numbers were significantly increased over controls by 24 h following challenge. In addition, rats passively sensitized for 72 h with anti-DNP IgE hybridoma antibody (PCA = 1:10,000) were challenged with DNP-BSA aerosols. Examination of BAL fluid 1 to 2 h following challenge revealed significantly increased numbers of PMNs which returned to normal levels by 24 h. Numbers of lymphocytes and macrophages were unchanged compared to controls. Microscopic examination of lung tissue revealed alveolar and interstitial edema at 2 h following challenge and a focal peribronchiolitis characterized by a predominantly mononuclear cell infiltrate.(ABSTRACT TRUNCATED AT 250 WORDS)