Roles of Iron Complexes in Catalytic Radical Alkene Cross-Coupling: A Computational and Mechanistic Study.

A growing and useful class of alkene coupling reactions involve hydrogen atom transfer (HAT) from a metal-hydride species to an alkene to form a free radical, which is responsible for subsequent bond formation. Here, we use a combination of experimental and computational investigations to map out the mechanistic details of iron-catalyzed reductive alkene cross-coupling, an important representative of the HAT alkene reactions. We are able to explain several observations that were previously mysterious. First, the rate-limiting step in the catalytic cycle is the formation of the reactive Fe-H intermediate, elucidating the importance of the choice of reductant. Second, the success of the catalytic system is attributable to the exceptionally weak (17 kcal/mol) Fe-H bond, which performs irreversible HAT to alkenes in contrast to previous studies on isolable hydride complexes where this addition was reversible. Third, the organic radical intermediates can reversibly form organometallic species, which helps to protect the free radicals from side reactions. Fourth, the previously accepted quenching of the postcoupling radical through stepwise electron transfer/proton transfer is not as favorable as alternative mechanisms. We find that there are two feasible pathways. One uses concerted proton-coupled electron transfer (PCET) from an iron(II) ethanol complex, which is facilitated because the O-H bond dissociation free energy is lowered by 30 kcal/mol upon metal binding. In an alternative pathway, an O-bound enolate-iron(III) complex undergoes proton shuttling from an iron-bound alcohol. These kinetic, spectroscopic, and computational studies identify key organometallic species and PCET steps that control selectivity and reactivity in metal-catalyzed HAT alkene coupling, and create a firm basis for elucidation of mechanisms in the growing class of HAT alkene cross-coupling reactions.

Catalyzed Radical Termination in the Presence of Tellanyl Radicals.

The decomposition of the diazo initiator dimethyl 2,2'-azobis(isobutyrate) (V-601), generating the Me2 C. (CO2 Me) radical, affords essentially the same fraction of disproportionation and combination in media with a large range of viscosity (C6 D6 , [D6 ]DMSO, and PEG 200) in the 25-100 °C range. This is in stark contrast to recent results by Yamago et al. on the same radical generated from Me2 C(TeMe)(CO2 Me) and on other X-TeR systems (X=polymer chain or unimer model; R=Me, Ph). The discrepancy is rationalized on the basis of an unprecedented RTe. -catalyzed radical disproportionation, with support from DFT calculations and photochemicaL V-601 decomposition in the presence of Te2 Ph2 .

Organometallic-Mediated Alternating Radical Copolymerization of tert-Butyl-2-Trifluoromethacrylate with Vinyl Acetate and Synthesis of Block Copolymers Thereof.

Organometallic-mediated radical polymerization (OMRP) has given access to well-defined poly(vinyl acetate-alt-tert-butyl-2-trifluoromethacrylate)-b-poly(vinyl acetate) and poly(VAc-alt-MAF-TBE) copolymers composed of two electronically distinct monomers: vinyl acetate (VAc, donor, D) and tert-butyl-2-trifluoromethacrylate (MAF-TBE, acceptor, A), with low dispersity (≤1.24) and molar masses up to 57 000 g mol-1 . These copolymers have a precise 1:1 alternating structure over a wide range of comonomer feed compositions. The reactivity ratios are determined as rVAc = 0.01 ± 0.01 and rMAF-TBE = 0 at 40 °C. Remarkably, from a feed containing >50% molar VAc content, poly(VAc-alt-MAF-TBE)-b-PVAc block copolymers are produced via a one-pot synthesis. Such diblock copolymers exhibit two glass transition temperatures attributed to the alternating and homopolymer sequences. The OMRP of this fluorine-containing alternating monomer system may provide access to a wide range of new polymer materials.

Direct mass measurements above uranium bridge the gap to the island of stability.

The mass of an atom incorporates all its constituents and their interactions. The difference between the mass of an atom and the sum of its building blocks (the binding energy) is a manifestation of Einstein's famous relation E = mc(2). The binding energy determines the energy available for nuclear reactions and decays (and thus the creation of elements by stellar nucleosynthesis), and holds the key to the fundamental question of how heavy the elements can be. Superheavy elements have been observed in challenging production experiments, but our present knowledge of the binding energy of these nuclides is based only on the detection of their decay products. The reconstruction from extended decay chains introduces uncertainties that render the interpretation difficult. Here we report direct mass measurements of trans-uranium nuclides. Located at the farthest tip of the actinide species on the proton number-neutron number diagram, these nuclides represent the gateway to the predicted island of stability. In particular, we have determined the mass values of (252-254)No (atomic number 102) with the Penning trap mass spectrometer SHIPTRAP. The uncertainties are of the order of 10 keV/c(2) (representing a relative precision of 0.05 p.p.m.), despite minute production rates of less than one atom per second. Our experiments advance direct mass measurements by ten atomic numbers with no loss in accuracy, and provide reliable anchor points en route to the island of stability.

Olefin oxygenation by water on an iridium center.

Oxygenation of 1,5-cyclooctadiene (COD) is achieved on an iridium center using water as a reagent. A hydrogen-bonding interaction with an unbound nitrogen atom of the naphthyridine-based ligand architecture promotes nucleophilic attack of water to the metal-bound COD. Irida-oxetane and oxo-irida-allyl compounds are isolated, products which are normally accessed from reactions with H2O2 or O2. DFT studies support a ligand-assisted water activation mechanism.

FAK-related nonkinase is a multifunctional negative regulator of pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a progressive fibrotic lung disease whose underlying molecular mechanisms are largely unknown. Herein, we show that focal adhesion kinase-related nonkinase (FRNK) plays a key role in limiting the development of lung fibrosis. Loss of FRNK function in vivo leads to increased lung fibrosis in an experimental mouse model. The increase in lung fibrosis is confirmed at the histological, biochemical, and physiological levels. Concordantly, loss of FRNK function results in increased fibroblast migration and myofibroblast differentiation and activation of signaling proteins that drive these phenotypes. FRNK-deficient murine lung fibroblasts also have an increased capacity to produce and contract matrix proteins. Restoration of FRNK expression in vivo and in vitro reverses these profibrotic phenotypes. These data demonstrate the multiple antifibrotic actions of FRNK. More important, FRNK expression is down-regulated in human IPF, and down-regulation of FRNK in normal human lung fibroblasts recapitulates the profibrotic phenotype seen in FRNK-deficient cells. The effect of loss and gain of FRNK in the experimental model, when taken together with its down-regulation in human IPF, suggests that FRNK acts as an endogenous negative regulator of lung fibrosis by repressing multiple profibrotic responses.

Metal-ligand cooperation on a diruthenium platform: selective imine formation through acceptorless dehydrogenative coupling of alcohols with amines.

Metal-metal singly-bonded diruthenium complexes, bridged by naphthyridine-functionalized N-heterocyclic carbene (NHC) ligands featuring a hydroxy appendage on the naphthyridine unit, are obtained in a single-pot reaction of [Ru2(CH3COO)2(CO)4] with 1-benzyl-3-(5,7-dimethyl-1,8-naphthyrid-2-yl)imidazolium bromide (BIN⋅HBr) or 1-isopropyl-3-(5,7-dimethyl-1,8-naphthyrid-2-yl)imidazolium bromide (PIN⋅HBr), TlBF4, and substituted benzaldehyde containing an electron-withdrawing group. The modified NHC-naphthyridine-hydroxy ligand spans the diruthenium unit in which the NHC carbon and hydroxy oxygen occupy the axial sites. All the synthesized compounds catalyze acceptorless dehydrogenation of alcohols to the corresponding aldehydes in the presence of a catalytic amount of weak base 1,4-diazabicyclo[2.2.2]octane (DABCO). Further, acceptorless dehydrogenative coupling (ADHC) of the alcohol with amines affords the corresponding imine as the sole product. The substrate scope is examined with 1 (BIN, p-nitrobenzaldehyde). A similar complex [Ru2(CO)4(CH3COO)(3-PhBIN)][Br], that is devoid of a hydroxy arm, is significantly less effective for the same reaction. Neutral complex 1 a, obtained by deprotonation of the hydroxy arm in 1, is found to be active for the ADHC of alcohols and amines under base-free conditions. A combination of control experiments, deuterium labeling, kinetic Hammett studies, and DFT calculations support metal-hydroxyl/hydroxide and metal-metal cooperation for alcohol activation and dehydrogenation. The bridging acetate plays a crucial role in allowing ß-hydride elimination to occur. The ligand architecture on the diruthenium core causes rapid aldehyde extrusion from the metal coordination sphere, which is responsible for exclusive imine formation.

Ru-Zn heteropolynuclear complexes containing a dinucleating bridging ligand: synthesis, structure, and isomerism.

Mononuclear complexes in- and out-[Ru(Cl)(trpy)(Hbpp)](+) (in-0, out-0; Hbpp is 2,2'-(1H-pyrazole-3,5-diyl)dipyridine and trpy is 2,2':6',2″-terpyridine) are used as starting materials for preparation of Ru-Zn heterodinuclear out-{[Ru(Cl)(trpy)][ZnCl2](µ-bpp)} (out-2) and heterotrinuclear in,in- and out,out-{[Ru(Cl)(trpy)]2(µ-[Zn(bpp)2])}(2+) (in-3, out-3) constitutional isomers. Further substitution of the Cl ligand from the former complexes leads to Ru-aqua out,out-{[Ru(trpy)(H2O)]2(µ-[Zn(bpp)2])}(4+) (out-4) and the oxo-bridged Ru-O-Ru complex in,in-{[Ru(III)(trpy)]2(µ-[Zn(bpp)2(H2O)]µ-(O)}(4+) (in-5). All complexes are thoroughly characterized by the usual analytical techniques as well as by spectroscopy by means of UV-vis, MS, and when diamagnetic NMR. CV and DPV are used to extract electrochemical information and monocrystal X-ray diffraction to characterize complexes out-2, in-3, out-3, and in-5 in the solid state. Complex out-3 photochemically isomerizes toward in-3, as can be observed by NMR spectroscopy and rationalized by density functional theory based calculations.

Reactions of acids with naphthyridine-functionalized ferrocenes: protonation and metal extrusion.

Reaction of 1,8-naphthyrid-2-yl-ferrocene (FcNP) with a variety of acids affords protonated salts at first, whereas longer reaction time leads to partial demetalation of FcNP resulting in a series of Fe complexes. The corresponding salts [FcNP·H][X] (X = BF(4) or CF(3)SO(3) (1)) are isolated for HBF(4) and CF(3)SO(3)H. Reaction of FcNP with equimolar amount of CF(3)CO(2)H for 12 h affords a neutral complex [Fe(FcNP)(2)(O(2)CCF(3))(2)(OH(2))(2)] (2). Use of excess acid gave a trinuclear Fe(II) complex [Fe(3)(H(2)O)(2)(O(2)CCF(3))(8)(FcNP·H)(2)] (3). Three linear iron atoms are held together by four bridging trifluoroacetates and two aqua ligands in a symmetric fashion. Reaction with ethereal solution of HCl afforded [(FcNP·H)(3)(Cl)][FeCl(4)](2) (4) irrespective of the amount of the acid used. Even the picric acid (HPic) led to metal extrusion giving rise to [Fe(2)(Cl)(2)(FcNP)(2)(Pic)(2)] (5) when crystallized from dichloromethane. Metal extrusion was also observed for CF(3)SO(3)H, but an analytically pure compound could not be isolated. The demetalation reaction proceeds with an initial proton attack to the distal nitrogen of the NP unit. Subsequently, coordination of the conjugate base to the electrophilic Fe facilitates the release of Cp rings from metal. The conjugate base plays an important role in the demetalation process and favors the isolation of the Fe complex as well. The 1,1'-bis(1,8-naphthyrid-2-yl)ferrocene (FcNP(2)) does not undergo demetalation under identical conditions. Two NP units share one positive charge causing the Fe-Cp bonds weakened to an extent that is not sufficient for demetalation. X-ray structure of the monoprotonated FcNP(2) reveals a discrete dimer [(FcNP(2)·H)](2)[OTf](2) (6) supported by two N-H···N hydrogen bonds. Crystal packing and dispersive forces associated with intra- and intermolecular π-π stacking interactions (NP···NP and Cp···NP) allow the formation of the dimer in the solid-state. The protonation and demetalation reactions of FcNP and FcNP(2) with a variety of acids are reported.

Two novel low molecular weight gelator-driven supramolecular metallogels efficient in antimicrobial activity applications.

A remarkable ultrasonication technique was successfully employed to create two novel metallogels using citric acid as a low molecular weight gelator, in combination with cadmium(ii)-acetate and mercury(ii)-acetate dissolved in N,N-dimethyl formamide at room temperature and under ambient conditions. The mechanical properties of the resulting Cd(ii)- and Hg(ii)-metallogels were rigorously examined through rheological analyses, which revealed their robust mechanical stability under varying angular frequencies and shear strains. Detailed characterization of the chemical constituents within these metallogels was accomplished through EDX mapping experiments, while microstructural features were visualized using field emission scanning electron microscope (FESEM) images. Additionally, FT-IR spectroscopic analysis was employed to elucidate the metallogel formation mechanism. Significantly, the antimicrobial efficacy of these novel metallogels was assessed against a panel of bacteria, including Gram-positive strains such as Bacillus subtilis and Staphylococcus epidermidis, as well as Gram-negative species like Escherichia coli and Pseudomonas aeruginosa. The results demonstrated substantial antibacterial activity, highlighting the potential of Cd(ii) and Hg(ii)-based citric acid-mediated metallogels as effective agents against a broad spectrum of bacteria. In conclusion, this study provides a comprehensive exploration of the synthesis, characterization, and antimicrobial properties of Cd(ii) and Hg(ii)-based citric acid-mediated metallogels, shedding light on their promising applications in combating both Gram-positive and Gram-negative bacterial infections. These findings open up exciting prospects for the development of advanced materials with multifaceted industrial and biomedical uses.

Exploration of a wide bandgap semiconducting supramolecular Mg(II)-metallohydrogel derived from an aliphatic amine: a robust resistive switching framework for brain-inspired computing.

A rapid metallohydrogelation strategy has been developed of magnesium(II)-ion using trimethylamine as a low molecular weight gelator in water medium at room temperature. The mechanical property of the synthesized metallohydrogel material is established through the rheological analysis. The nano-rose like morphological patterns of Mg(II)-metallohydrogel are characterized through field emission scanning electron microscopic study. The energy dispersive X-ray elemental mapping analysis confirms the primary gel forming elements of Mg(II)-metallohydrogel. The possible metallohydrogel formation strategy has been analyzed through FT-IR spectroscopic study. In this work, magnesium(II) metallohydrogel (Mg@TMA) based metal-semiconductor-metal structures have been developed and charge transport behaviour is studied. Here, it is confirmed that the magnesium(II) metallohydrogel (Mg@TMA) based resistive random access memory (RRAM) device is showing bipolar resistive switching behaviour at room temperature. We have also explored the mechanism of resistive switching behaviour using the formation (rupture) of conductive filaments between the metal electrodes. This RRAM devices exhibit excellent switching endurance over 10,000 switching cycles with a large ON/OFF ratio (~ 100). The easy fabrication techniques, robust resistive switching behaviour and stability of the present system makes these structures preferred candidate for applications in non-volatile memory design, neuromorphic computing, flexible electronics and optoelectronics etc.

Vav protein guanine nucleotide exchange factor regulates CD36 protein-mediated macrophage foam cell formation via calcium and dynamin-dependent processes.

Atherosclerosis, a chronic inflammatory disease, results in part from the accumulation of modified lipoproteins in the arterial wall and formation of lipid-laden macrophages, known as "foam cells." Recently, we reported that CD36, a scavenger receptor, contributes to activation of Vav-family guanine nucleotide exchange factors by oxidatively modified LDL in macrophages. We also discovered that CD36-dependent uptake of oxidized LDL (oxLDL) in vitro and foam cell formation in vitro and in vivo was significantly reduced in macrophages deficient of Vav proteins. The goal of the present study was to identify the mechanisms by which Vav proteins regulate CD36-dependent foam cell formation. We now show that a Vav-dynamin signaling axis plays a critical role in generating calcium signals in mouse macrophages exposed to CD36-specific oxidized phospholipid ligands. Chelation of intracellular Ca(2+) or inhibition of phospholipase C-γ (PLC-γ) inhibited Vav activation (85 and 70%, respectively, compared with vehicle control) and reduced foam cell formation (approximately 75%). Knockdown of expression by siRNA or inhibition of GTPase activity of dynamin 2, a Vav-interacting protein involved in endocytic vesicle fission, significantly blocked oxLDL uptake and inhibited foam cell formation. Immunofluorescence microscopy studies showed that Vav1 and dynamin 2 colocalized with internalized oxLDL in macrophages and that activation and mobilization of dynamin 2 by oxLDL was impaired in vav null cells. These studies identified previously unknown components of the CD36 signaling pathway, demonstrating that Vav proteins regulate oxLDL uptake and foam cell formation via calcium- and dynamin 2-dependent processes and thus represent novel therapeutic targets for atherosclerosis.

Vav family Rho guanine nucleotide exchange factors regulate CD36-mediated macrophage foam cell formation.

Lipid-laden macrophages or "foam cells" are the primary components of the fatty streak, the earliest atherosclerotic lesion. Although Vav family guanine nucleotide exchange factors impact processes highly relevant to atherogenesis and are involved in pathways common to scavenger receptor CD36 signaling, their role in CD36-dependent macrophage foam cell formation remains unknown. The goal of the present study was to determine the contribution of Vav proteins to CD36-dependent foam cell formation and to identify the mechanisms by which Vavs participate in the process. We found that CD36 contributes to activation of Vav-1, -2, and -3 in aortae from hyperlipidemic mice and that oxidatively modified LDL (oxLDL) induces activation of macrophage Vav in vitro in a CD36 and Src family kinase-dependent manner. CD36-dependent uptake of oxLDL in vitro and foam cell formation in vitro and in vivo was significantly reduced in Vav null macrophages. These studies for the first time link CD36 and Vavs in a signaling pathway required for macrophage foam cell formation.

Ligand-bridged dinuclear cyclometalated Ir(III) complexes: from metallamacrocycles to discrete dimers.

Metallamacrocycles 1, 2, and 3 of the general formula [{Ir(ppy)(2)}(2)(µ-BL)(2)](OTf)(2) (ppyH = 2-phenyl pyridine; BL = 1,2-bis(4-pyridyl)ethane (bpa) (1), 1,3-bis(4-pyridyl)propane (bpp) (2), and trans-1,2-bis(4-pyridyl)ethylene (bpe) (3)) have been synthesized by the reaction of [{(ppy)(2)Ir}(2)(µ-Cl)(2)], first with AgOTf to effect dechlorination and later with various bridging ligands. Open-frame dimers [{Ir(ppy)(2)}(2)(µ-BL)](OTf)(2) were obtained in a similar manner by utilizing N,N'-bis(2-pyridyl)methylene-hydrazine (abp) and N,N'-(bis(2-pyridyl)formylidene)ethane-1,2-diamine (bpfd) (for compounds 4 and 5, respectively) as bridging ligands. Molecular structures of 1, 3, 4, and 5 were established by X-ray crystallography. Cyclic voltammetry experiments reveal weakly interacting "Ir(ppy)(2)" units bridged by ethylene-linked bpe ligand in 3; on the contrary the metal centers are electronically isolated in 1 and 2 where the bridging ligands are based on ethane and propane linkers. The dimer 4 exhibits two accessible reversible reduction couples separated by 570 mV indicating the stability of the one-electron reduced species located on the diimine-based bridge abp. The "Ir(ppy)(2)" units in compound 5 are noninteracting as the electronic conduit is truncated by the ethane spacer in the bpfd bridge. The dinuclear compounds 1-5 show ligand centered (LC) transitions involving ppy ligands and mixed metal to ligand/ligand to ligand charge transfer (MLCT/LLCT) transitions involving both the cyclometalating ppy and bridging ligands (BL) in the UV-vis spectra. For the conjugated bridge bpe in compound 3 and abp in compound 4, the lowest-energy charge-transfer absorptions are red-shifted with enhanced intensity. In accordance with their similar electronic structures, compounds 1 and 2 exhibit identical emissions. The presence of vibronic structures in these compounds indicates a predominantly (3)LC excited states. On the contrary, broad and unstructured phosphorescence bands in compounds 3-5 strongly suggest emissive states of mixed (3)MLCT/(3)LLCT character. Density functional theory (DFT) calculations have been carried out to gain insight on the frontier orbitals, and to rationalize the electrochemical and photophysical properties of the compounds based on their electronic structures.

A CD36-dependent signaling cascade is necessary for macrophage foam cell formation.

Accumulation of macrophage foam cells in atherosclerotic blood vessel intima is a critical component of atherogenesis mediated by scavenger receptor-dependent internalization of oxidized LDL. We demonstrated by coimmunoprecipitation and pull-down assays that the macrophage scavenger receptor CD36 associates with a signaling complex containing Lyn and MEKK2. The MAP kinases JNK1 and JNK2 were specifically phosphorylated in macrophages exposed to oxLDL. Using cells isolated from SRA, TLR2, or CD36 null mice, and phospholipid ligands specific for either SRA or CD36, we showed that JNK activation was mediated by CD36. Both foam cell formation and activation of JNK2 in hyperlipidemic mice were diminished in the absence of CD36. Furthermore, inhibition of Src or JNK blocked oxLDL uptake and inhibited foam cell formation in vitro and in vivo. These findings show that a specific CD36-dependent signaling pathway initiated by oxLDL is necessary for foam cell formation and identify potential targets for antiatherosclerosis therapy.

Mass measurements of very neutron-deficient Mo and Tc isotopes and their impact on rp process nucleosynthesis.

The masses of ten proton-rich nuclides, including the N=Z+1 nuclides 85Mo and 87Tc, were measured with the Penning trap mass spectrometer SHIPTRAP. Compared to the Atomic Mass Evaluation 2003 a systematic shift of the mass surface by up to 1.6 MeV is observed causing significant abundance changes of the ashes of astrophysical x-ray bursts. Surprisingly low α separation energies for neutron-deficient Mo and Tc are found, making the formation of a ZrNb cycle in the rp process possible. Such a cycle would impose an upper temperature limit for the synthesis of elements beyond Nb in the rp process.

Reactor decay heat in 239Pu: solving the γ discrepancy in the 4-3000-s cooling period.

The ß feeding probability of (102,104,105,106,107)Tc, 105Mo, and 101Nb nuclei, which are important contributors to the decay heat in nuclear reactors, has been measured using the total absorption technique. We have coupled for the first time a total absorption spectrometer to a Penning trap in order to obtain sources of very high isobaric purity. Our results solve a significant part of a long-standing discrepancy in the γ component of the decay heat for 239Pu in the 4-3000 s range.

Bimetallic catalysis involving dipalladium(I) and diruthenium(I) complexes.

Dipalladium(I) and diruthenium(I) compounds bridged by two [{(5,7-dimethyl-1,8-naphthyridin-2-yl)amino}carbonyl]ferrocene (L) ligands have been synthesized. The X-ray structures of [Pd(2)L(2)][BF(4)](2) (1) and [Ru(2)L(2)(CO)(4)][BF(4)](2) (2) reveal dinuclear structures with short metal-metal distances. In both of these structures, naphthyridine bridges the dimetal unit, and the site trans to the metal-metal bond is occupied by weakly coordinating oxygen from the amido fragment. The catalytic utilities of these bimetallic compounds are evaluated. Compound 1 is an excellent catalyst for phosphine-free, Suzuki cross-coupling reactions of aryl bromides with arylboronic acids and provides high yields in short reaction times. Compound 1 is also found to be catalytically active for aryl chlorides, although the corresponding yields are lower. A bimetallic mechanism is proposed, which involves the oxidative addition of aryl bromide across the Pd-Pd bond and the bimetallic reductive elimination of the product. Compound 1 is also an efficient catalyst for the Heck cross-coupling of aryl bromides with styrenes. The mechanism for aldehyde olefination with ethyl diazoacetate (EDA) and PPh(3), catalyzed by 2, has been fully elucidated. It is demonstrated that 2 catalyzes the formation of phosphorane utilizing EDA and PPh(3), which subsequently reacts with aldehyde to produce a new olefin and phosphine oxide. The efficacy of bimetallic complexes in catalytic organic transformations is illustrated in this work.

Mapping the transformation [{Ru(II)(CO)(3)Cl(2)}(2)]-->[Ru(I) (2)(CO)(4)](2+): implications in binuclear water-gas shift chemistry.

The complete sequence of reactions in the base-promoted reduction of [{Ru(II)(CO)(3)Cl(2)}(2)] to [Ru(I) (2)(CO)(4)](2+) has been unraveled. Several mu-OH, mu:kappa(2)-CO(2)H-bridged diruthenium(II) complexes have been synthesized; they are the direct results of the nucleophilic activation of metal-coordinated carbonyls by hydroxides. The isolated compounds are [Ru(2)(CO)(4)(mu:kappa(2)-C,O-CO(2)H)(2)(mu-OH)(NP(F)-Am)(2)][PF(6)] (1; NP(F)-Am=2-amino-5,7-trifluoromethyl-1,8-naphthyridine) and [Ru(2)(CO)(4)(mu:kappa(2)-C,O-CO(2)H)(mu-OH)(NP-Me(2))(2)][BF(4)](2) (2), secured by the applications of naphthyridine derivatives. In the absence of any capping ligand, a tetranuclear complex [Ru(4)(CO)(8)(H(2)O)(2)(mu(3)-OH)(2)(mu:kappa(2)-C,O-CO(2)H)(4)][CF(3)SO(3)](2) (3) is isolated. The bridging hydroxido ligand in 1 is readily replaced by a pi-donor chlorido ligand, which results in [Ru(2)(CO)(4)(mu:kappa(2)-C,O-CO(2)H)(2)(mu-Cl)(NP-PhOMe)(2)][BF(4)] (4). The production of [Ru(2)(CO)(4)](2+) has been attributed to the thermally induced decarboxylation of a bis(hydroxycarbonyl)-diruthenium(II) complex to a dihydrido-diruthenium(II) species, followed by dinuclear reductive elimination of molecular hydrogen with the concomitant formation of the Ru(I)--Ru(I) single bond. This work was originally instituted to find a reliable synthetic protocol for the [Ru(2)(CO)(4)(CH(3)CN)(6)](2+) precursor. It is herein prescribed that at least four equivalents of base, complete removal of chlorido ligands by Tl(I) salts, and heating at reflux in acetonitrile for a period of four hours are the conditions for the optimal conversion. Premature quenching of the reaction resulted in the isolation of a trinuclear Ru(I) (2)Ru(II) complex [{Ru(NP-Am)(2)(CO)}{Ru(2)(NP-Am)(2)(CO)(2)(mu-CO)(2)}(mu(3):kappa(3)-C,O,O'-CO(2))][BF(4)](2) (6). These unprecedented diruthenium compounds are the dinuclear congeners of the water-gas shift (WGS) intermediates. The possibility of a dinuclear pathway eliminates the inherent contradiction of pH demands in the WGS catalytic cycle in an alkaline medium. A cooperative binuclear elimination could be a viable route for hydrogen production in WGS chemistry.

Mechanisms of cell signaling by the scavenger receptor CD36: implications in atherosclerosis and thrombosis.

CD36 is a multifunctional membrane receptor present on mononuclear phagocytes, platelets, and other cells that serves as a scavenger receptor for oxidized phospholipids, apoptotic cells and certain microbial pathogens. On macrophages, CD36 interaction with oxidized LDL (oxLDL) triggers a signaling response that is pro-inflammatory and pro-atherogenic. The signaling pathway involves activation of src-family kinases, MAP kinases, and Vav family guanine nucleotide exchange factors and results in ligand internalization, foam cell formation and inhibition of migration. On platelets, CD36 interaction with oxLDL and cell-derived microparticles transduces intracellular signals that render them more reactive to low concentrations of classical agonists. In vitro studies and in vivo experiments in CD36 null mice have revealed an important mechanistic role for CD36 in atherosclerosis and thrombosis. Identification of the precise CD36 signaling pathways in specific cells elicited in response to specific ligands may yield novel targets for drug development in athero-thrombotic disorders.