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Many transition-metal complexes MLn decompose diazo compounds N2-CR1R2 generating metal-carbenes LnM-CR1R2 which transfer the carbene group to other substrates, constituting an important tool in organic synthesis. All previous reports have shown that the CR1R2 fragment at the metal-carbene remains intact from the parent diazo compound. Herein we report the detection and isolation of a monosubstituted copper carbene where the CR1R2 ligand has undergone a modification from the initial diazo reagent. When TpMsCu(THF) (TpMs = hydrotris(3-mesityl)pyrazolylborate ligand) was reacted with N,N-diethyl diazoacetamide [N2-C(H)(CONEt2)], the stable copper carbene TpMsCu-C(H)(NEt2) was isolated, resulting from a decarbonylation process, with carbon monoxide being trapped as TpMsCu(CO). The simultaneous observation of products derived from the intramolecular carbene insertion reaction into C–H bonds demonstrates that the expected TpMsCu-C(H)(CONEt2) complex is also formed. Experimental data, DFT calculations, and microkinetic models allow us to propose that the latter undergoes CO loss en route to the former., Funding for open access charge: Universidad de Huelva / CBUA, Funding for open access charge: Universidad de Huelva / CBUAWe dedicate this work to the memory of Professor Victor Riera, one of the pioneers of organometallic chemistry in Spain. We acknowledge financial support from the Ministerio de Ciencia e Innovación (CTQ2017-82893-C2-1-R, CTQ2017- 87792-R, P. O. Feder UHU-1260216 and P. O. Feder UHU- 1254043, and Red Intecat CTQ2016-81923-REDC)

Nitrogen (N) management is important for farmers to balance production, economic and environmental performance of their farms. This is particularly true in the intensive cropping systems of northwest Europe where tuber, root and bulb crops are cultivated in rotation with cereal crops and where an intensive livestock sector makes organic manures available at low cost for arable farmers. Here, we build upon a large database of farmer field data to assess mineral and organic fertiliser N performance, and its determinants, for the major arable crops in the Netherlands according to the guidelines provided by the EU N Expert Panel (EUNEP). The EUNEP framework quantifies N outputs and N inputs, N-use efficiency as the ratio between N outputs and N inputs (NUE in kg N output harvested per kg N input) and N surplus as the difference between N inputs and N outputs (Ns in kg N ha−1). As a next step, biophysical and crop management determinants of N performance were explored using data from different years, soil types and N management in relation to the amount, source, time and method of N applied. NUE was on average ca. 0.95 kg N kg−1 N for seed potato, sugar beet and spring onion, 0.87 kg N kg−1 N for ware potato, ca. 0.80 kg N kg−1 N for starch potato and winter wheat and, ca. 0.70 kg N kg−1 N for spring barley, all within or above the target range of 0.50–0.90 kg N kg−1 N proposed by the EUNEP. Ns was on average below the EUNEP threshold of 80 kg N ha−1 for all crops: 78 kg N ha−1 for ware potato and winter wheat, ca. 70 kg N ha−1 for starch potato, ca. 50 kg N ha−1 for spring barley, ca. 25 kg N ha−1 for sugar beet and spring onion and less than 20 kg N ha−1 for seed potato. Although average Ns was below 80 kg N ha−1, ca. 40% of the ware potato, starch potato and winter wheat fields analyzed had Ns above this threshold. The relatively high NUE combined with high Ns for most crops are the result of high N outputs (yields) combined with high N application rates. Moreover, high NUE and small Ns were mostly associated with smaller N application rates and with the use of mineral fertilisers instead of organic fertilisers, while there were no clear relationships between the two indicators on the one hand with N application time or method on the other. We conclude NUE and Ns were on average within the EUNEP target range for most crops, but there are still a considerable number of under-performing farms where increases in NUE and reductions in Ns are possible through reducing N inputs. We recommend future research to assess the benefits of organic fertilisers from a circularity perspective at regional and national levels and to cross-validate the crop-specific results presented in this study with NUE assessments at cropping systems level., This research was conducted as part of the WaterFARMING project “Improvement of water and nutrient retention and use efficiency in arable farming systems from field to catchment scale in Europe and North Africa” funded by the Netherlands Science Foundation (NWO) with grant agreement ALWWW20161.

Here we present new information on the shape evolution of the very neutron-rich ^{92,94}Se nuclei from an isomer-decay spectroscopy experiment at the Radioactive Isotope Beam Factory at RIKEN. High-resolution germanium detectors were used to identify delayed γ rays emitted following the decay of their isomers. New transitions are reported extending the previously known level schemes. The isomeric levels are interpreted as originating from high-K quasineutron states with an oblate deformation of β∼0.25, with the high-K state in ^{94}Se being metastable and K hindered. Following this, ^{94}Se is the lowest-mass neutron-rich nucleus known to date with such a substantial K hindrance. Furthermore, it is the first observation of an oblate K isomer in a deformed nucleus. This opens up the possibility for a new region of K isomers at low Z and at oblate deformation, involving the same neutron orbitals as the prolate orbitals within the classic Z∼72 deformed hafnium region. From an interpretation of the level scheme guided by theoretical calculations, an oblate deformation is also suggested for the ^{94}Se_{60} ground-state band.

This article presents new joining-by-forming processes to assemble longitudinally two metal–polymer sandwich composite panels perpendicular to one another. Process design draws from an earlier development of the authors for metal sheets to new concepts based on the combination of sheet-bulk forming with mortise-and-tenon joints. Selected examples obtained from experimentation and finite element modelling give support to the presentation. A new three-stage joining by the forming process is capable of producing mechanically locked joints with larger and stiffer flat-shaped heads than those fabricated by alternative single- or two-stage solutions. Failure in the new three-stage joining by the forming process is found to take place by cracking instead of disassembling after unbending the flat-shaped head of the joint back to its original shape. The required forming forces to produce the new metal–polymer joints are below 15 kN, allowing them to be an effective, easy-to-implement alternative to existing solutions based on adhesive bonding, welding and mechanical fastening.

A multigram method for the preparation of thallium trispyrazolylborate complexes is described., The authors wish to thank MINECO for financial support (CTQ2014-52769-C03-01 and CTQ2015-73693-JIN). A.P. thanks MEC for the FPU fellowship.

Nickel catalysis is gaining in popularity in recent years, mostly within the area of cross-coupling. However, unlike Pd, the mechanisms of Ni-catalyzed C–C and C–heteroatom bond forming reactions have been much less studied, in particular when N-heterocyclic carbenes are used as ligands. Here, we present a thorough study of the mechanism of C–N cross-coupling reactions catalyzed by an NHC-Ni complex. Focusing on the coupling of 2-chloropyridines with indole catalyzed by [(IPrNi(styrene)2] (IPr = N,N′-bis(2,6-diisopropylphenyl)imidazol-2-ylidene), we have examined each of the elementary steps: i.e., oxidative addition, ligand substitution, and reductive elimination. All relevant catalytic intermediates have been isolated and structurally characterized by both spectroscopic and crystallographic methods. Kinetic studies have revealed that the reductive elimination is the rate-limiting step. Catalyst deactivation is related to the formation of unproductive dinuclear pyridyl-bridged NHC-NiII species, which can...

Two iridium(III) complexes containing a C,N-bidentate pyridyl-triazolylidene ligand were prepared that are structurally very similar but differ in their pendant substituent. Whereas complex 1 contains a non-coordinating pyridyl unit, complex 2 has a phenyl group on the triazolylidene substituent. The presence of the basic pyridyl unit has distinct effects on the catalytic activity of the complex in the oxidative dehydrogenation of benzylic amines, inducing generally higher rates, higher selectivity towards formation of imines versus secondary amines, and notable quantities of tertiary amines when compared to the phenyl-functionalized analogue. The role of the pyridyl functionality has been elucidated from a set of stoichiometric experiments, which demonstrate hydrogen bonding between the pendant pyridyl unit and the amine protons of the substrate. Such Npyr···H-N interactions are demonstrated by X-ray diffraction analysis, 1H NMR, and IR spectroscopy, and suggest a pathway of substrate bond-activation that involves concerted substrate binding through the Lewis acidic iridium center and the Lewis basic pyridyl site appended to the triazolylidene ligand, in agreement with ligand–metal cooperative substrate activation.

Methane emissions have very important effect on global radiative forcing. Therefore, reducing these emissions has been proposed as an effective short-term strategy to mitigate global warming, in parallel with reductions in long-lived carbon dioxide (CO 2 ) for long-term temperature stabilizations. In this context, Argentina emits 3645 Gg of CH 4 mainly from livestock production, biomass burning and natural gas production. Since 2018, TROPOMI instruments provide global coverage on methane column-average mole fraction of dry air (XCH 4 ), and height profiles of methane concentrations. We compare two available methane inventory: a national (a high resolution of own ellaboration: GEAA) and an international (EDGAR) emissions database with TROPOMI measurements. By performing inverse satellite retrieval we evaluate the ability of remote sensing information to detect possible hotspot methane emissions and compare these results with the two inventories. From these analyzes, we observe that the latitudinal averages of the continental sector increase at a rate of 10 ppb/degree, from south to north, while the maritime sector remains constant. From a temporary perspective, the average monthly concentration amplitude range varies 40 to 50 ppb, with minimum values in March and maximum values in September.

Background: Shape coexistence in the Z≈82 region has been established in mercury, lead, and polonium isotopes. For even-even mercury isotopes with 100≤N≤106 multiple fingerprints of this phenomenon are observed, which seems to be no longer present for N≥110. According to a number of theoretical calculations, shape coexistence is predicted in the Hg188 isotope. Purpose: The aim of this work was to measure lifetimes of excited states in Hg188 to infer their collective properties, such as the deformation. Extending the investigation to higher-spin states, which are expected to be less affected by band-mixing effects, can provide additional information on the coexisting structures. Methods: The Hg188 nucleus was populated using two different fusion-evaporation reactions with two targets, Gd158 and Gd160, and a beam of S34 provided by the Tandem-ALPI accelerator complex at the Laboratori Nazionali di Legnaro. The channels of interest were selected using the information from the Neutron Wall array, while the γ rays were detected using the GALILEO γ-ray spectrometer. Lifetimes of excited states were determined using the recoil-distance Doppler-shift method, employing the dedicated GALILEO plunger device. Results: Lifetimes of the states up to spin 16ℏ were measured and the corresponding reduced transition probabilities were calculated. Assuming two-band mixing and adopting, as done commonly, the rotational model, the mixing strengths and the deformation parameters of the unperturbed structures were obtained from the experimental results. In order to shed light on the nature of the observed configurations in the Hg188 nucleus, the extracted transition strengths were compared with those resulting from state-of-the-art beyond-mean-field calculations using the symmetry-conserving configuration-mixing approach, limited to axial shapes, and the five-dimensional collective Hamiltonian, including the triaxial degree of freedom. Conclusions: The first lifetime measurement for states with spin ≥6 suggested the presence of an almost spherical structure above the 121+ isomer and allowed elucidating the structure of the intruder band. The comparison of the extracted B(E2) strengths with the two-band mixing model allowed the determination of the ground-state band deformation. Both beyond-mean-field calculations predict coexistence of a weakly deformed band with a strongly prolate-deformed one, characterized by elongation parameters similar to those obtained experimentally, but the calculated relative position of the bands and their mixing strongly differ.

The mild generation of nitrogen-centred radicals from N–F reagents has become a convenient synthetic tool. This methodology provides access to the aminative difunctionalisation of alkenes and alkynes and the radical ring-opening of cyclopropanes, among other similar transformations. This review article aims to provide an overview of recent developments of such processes involving radical reactions and N–F reagents using copper-based catalysts., We thank Ministerio de Economía y Competitividad (MINECO) (CTQ2017-82893-C2-1-R) and Universidad de Huelva (PO FEDER 2014-2020 UHU-1254043) for grants.

In the brain neuropil, translocator protein 18 kDa (TSPO) is a stress response protein that is upregulated in microglia and astrocytes in diverse central nervous system pathologies. TSPO is widely used as a biomarker of neuroinflammation in preclinical and clinical neuroimaging studies. However, there is a paucity of knowledge on the function(s) of TSPO in glial cells. In this study, we explored a putative interaction between TSPO and NADPH oxidase 2 (NOX2) in microglia. We found that TSPO associates with gp91phox and p22phox, the principal subunits of NOX2 in primary murine microglia. The association of TSPO with gp91phox and p22phox was observed using co-immunoprecipitation, confocal immunofluorescence imaging, and proximity ligation assay. We found that besides gp91phox and p22phox, voltage-dependent anion channel (VDAC) also co-immunoprecipitated with TSPO consistent with previous reports. When we compared lipopolysaccharide (LPS) stimulated microglia to vehicle control, we found that a lower amount of gp91phox and p22phox protein co-immunoprecipitated with TSPO suggesting a disruption of the TSPO-NOX2 subunits association. TSPO immuno-gold electron microscopy confirmed that TSPO is present in the outer mitochondrial membrane but it is also found in the endoplasmic reticulum (ER), mitochondria-associated ER membrane (MAM), and in the plasma membrane. TSPO localization at the MAM may represent a subcellular site where TSPO interacts with gp91phox and p22phox since the MAM is a point of communication between outer mitochondria membrane proteins (TSPO) and ER proteins (gp91phox and p22phox) where they mature and form the cytochrome b558 (Cytb558) heterodimer. We also found that an acute burst of reactive oxygen species (ROS) increased TSPO levels on the surface of microglia and this effect was abrogated by a ROS scavenger. These results suggest that ROS production may alter the subcellular distribution of TSPO. Collectively, our findings suggest that in microglia, TSPO is associated with the major NOX2 subunits gp91phox and p22phox. We hypothesize that this interaction may regulate Cytb558 formation and modulate NOX2 levels, ROS production, and redox homeostasis in microglia.

Background: The neutron-deficient osmium isotopic chain provides a great laboratory for the study of shape evolution, with the transition from the soft triaxial rotor in $^{168}\mathrm{Os}$ to the well-deformed prolate rotor in $^{180}\mathrm{Os}$, while shape coexistence appears around $N=96$ in $^{172}\mathrm{Os}$. Therefore, the study of the Os isotopic chain should provide a better understanding of shape changes in nuclei and a detailed scrutiny of nuclear structure calculations. In this paper, the lifetimes of the low-lying yrast states of $^{170}\mathrm{Os}$ have been measured for the first time to investigate the shape evolution with neutron number.Purpose: Lifetimes of excited states in the ground-state band of $^{170}\mathrm{Os}$ are measured to investigate the shape evolution with neutron number in osmium isotopes and compare with state-of-the-art calculations.Methods: The states of interest were populated via the fusion-evaporation reaction $^{142}\mathrm{Nd}(^{32}\mathrm{S},4n)$ at a bombarding energy of 170 MeV at the ALTO facility from IPN (Orsay, France). Lifetimes of the ${2}_{1}^{+}$ and ${4}_{1}^{+}$ states in $^{170}\mathrm{Os}$ were measured with the recoil-distance Doppler-shift method using the Orsay universal plunger system.Results: Lifetimes of the two first excited states in $^{170}\mathrm{Os}$ were measured for the first time. A very small $B(E2;{4}_{1}^{+}\ensuremath{\rightarrow}{2}_{1}^{+})/B(E2;{2}_{1}^{+}\ensuremath{\rightarrow}{0}_{1}^{+})=0.38(11)$ was found, which is very uncharacteristic for collective nuclei. These results were compared to state-of-the-art beyond-mean-field calculations.Conclusions: Although theoretical results give satisfactory results for the energy of the first few excited states in $^{170}\mathrm{Os}$ and the $B(E2;{2}_{1}^{+}\ensuremath{\rightarrow}{0}_{1}^{+})$ they fail to reproduce the very small $B(E2;{4}_{1}^{+}\ensuremath{\rightarrow}{2}_{1}^{+})$, which remains a puzzle.

Tris(pyrazolyl)methane ligands (Tpmx) have been for years a step behind their highly popular boron-anionic analogues, the tris(pyrazolyl)borate ligands (Tpx). However, in the last decade the development of new members of this family of ligands has boosted a number of contributions albeit their use in coordination chemistry. This fact has also triggered the application of metal-Tpmx complexes as catalysts for a range of organic transformations, particularly with group 11 metals. The main structural features of complexes containing the TpmxM (M = Cu, Ag, Au) unit and their success as catalysts in a variety of reactions under homogeneous or heterogeneous conditions are presented., We thank MINECO for support with Grant CTQ2017-82893-C2-1-R

The dual function of the N-F bond as an effective oxidant and subsequent nitrogen source in intramolecular aliphatic C-H functionalization reactions is explored. Copper catalysis is demonstrated to exercise full regio- and chemoselectivity control, which opens new synthetic avenues to nitrogenated heterocycles with predictable ring sizes. For the first time, a uniform catalysis manifold has been identified for the construction of both pyrrolidine and piperidine cores. The individual steps of this new copper oxidation catalysis were elucidated by control experiments and computational studies, clarifying the singularity of the N-F function and characterizing the catalytic cycle to be based on a copper(I/II) manifold., We thank MINECO for Grants CTQ2017-82893-C2-1-R, CTQ2017-87792-R, CTQ2017-88496-R, COST Action CA15106 “C–H Activation in Organic Synthesis (CHAOS)”and Red Intecat (CTQ2016-81923-REDC).

In addition to increased morbidity and mortality caused by respiratory and cardiovascular diseases, air pollution may also contribute to central nervous system (CNS) diseases. Traffic-related air pollution is a major contributor to global air pollution, and diesel exhaust (DE) is its most important component. DE contains more than 40 toxic air pollutants and is a major constituent of ambient particulate matter (PM), particularly of ultrafine-PM. Limited information suggest that exposure to DE may cause oxidative stress and neuroinflammation in the CNS. We hypothesized that males may be more susceptible than females to DE neurotoxicity, because of a lower level of expression of paraoxonase 2 (PON2), an intracellular anti-oxidant and anti-inflammatory enzyme. Acute exposure of C57BL/6 mice to DE (250–300 µg/m3 for 6h) caused significant increases in lipid peroxidation and of pro-inflammatory cytokines (IL-1α, IL-1β, IL-3, IL-6, TNF-α) in various brain regions (particularly olfactory bulb and hippocampus). In a number of cases the observed effects were more pronounced in male than in female mice. DE exposure also caused microglia activation, as measured by increased Iba1 (ionized calcium-binding adapter molecule 1) expression, and of TSPO (translocator protein) binding. Mice heterozygotes for the modifier subunit of glutamate cysteine ligase (the limiting enzyme in glutathione biosynthesis; Gclm+/− mice) appeared to be significantly more susceptible to DE-induced neuroinflammation than wild type mice. These findings indicate that acute exposure to DE causes neuroinflammation and oxidative stress in brain, and suggests that sex and genetic background may play important roles in modulating susceptibility to DE neurotoxicity.

During the past decade, translocator protein 18 kDa (TSPO), previously named peripheral benzodiazepine receptor, has gained a great deal of attention based on its use as a clinical biomarker of neuroinflammation with therapeutic potential. However, there is a paucity of knowledge on the function(s) of TSPO in glial cells. Here, we identify a novel function of TSPO in microglia that is not associated with steroidogenesis. We propose that a TSPO interaction with NADPH oxidase (NOX2) links the generation of reactive oxygen species (ROS) to the induction of an antioxidant response to maintain redox homeostasis. This line of investigation may provide a greater understanding of TSPO glial cell biology, and the knowledge gained may prove beneficial in devising therapeutic strategies.

Tris(pyrazolyl)borates (Tpx) have become one of the most broadly used polydentate anionic ligands in coordination chemistry and catalysis since Trofimenko introduced them in 1966. Herein we present a review of the main structural features of Group 11 metal complexes with Tpx ligands, as well as their catalytic properties, can be controlled by ligand steric and electronic factors., We thank MINECO for funding (Grant CTQ2017-82893-C2-1-R).We thank MINECO for Grant CTQ2017-82893-C2-1-R.

Statistical treatment of experimental 13 C NMR chemical shifts of different compounds and calculated isotropic shielding constants of their respective conformers has been carried out in two different ways. The first method was a ridge linear regression between experimental chemical shifts and calculated shielding constants where the calculated coefficients represent the mole fraction of each conformer. Consequently, the sum of all coefficients has to be restricted to 1. The second method was a linear regression between experimental and calculated internal chemical shifts using the same restriction. In general, both methods gave similar results although the second one had a larger standard deviation. The results showed that, in nearly all cases, there is a significant correlation between experimental and calculated data for, at least, one conformer, being this the major one present in the conformational equilibrium. For planar aromatic compounds the conformational equilibrium has been fully characterized when other conformers have been found statistically significant. The statistical analysis on cyclic aliphatic molecules always yielded a conformational composition comparable with the published values. The advantages and drawbacks of the methodology are discussed.

The electrochemical 2-fold dehalogenation of a spirocyclopropane-proline derivative at leaded bronze was scaled-up in a divided batch-type electrolysis cell in good yield and excellent selectivity. The upscaling via a flow electrolysis cell was also successful. Conditions were elaborated employing a single cell passage for complete conversion. The keys here are the direct cooling of the cathode and ensuring a good laminar flow.

The functionalization of the primary sites of alkanes is one of the more challenging areas in catalysis. In this context, a novel effect has been discovered that is responsible for an enhancement in the reactivity of the primary C-H bonds of alkanes in a catalytic system. The copper complex Cu(NCMe) (=hydrotris{[3,5-bis(trifluoromethyl)-4-bromo]-pyrazol-1-yl}borate) catalyzes the functionalization of CnH2n+2 with ethyl diazoacetate upon inserting the CHCO2Et unit into C-H bonds. In addition, the selectivity of the reaction toward the primary sites significantly increased relative to that obtained in neat alkane upon using supercritical carbon dioxide as the reaction medium. This was attributed to the effect of the carbon dioxide molecules that withdraw electron density from the fluorine atoms of the ligand, which enhances the electrophilic nature of the metal center. DFT studies validated this proposal.

The copper complex Tp(CF3)2,BrCu(NCMe) (1, Tp(CF3)2,Br = hydrotris((3,5-bis(trifluoromethyl)-4-bromo)-pyrazol-1-yl)borate) catalyzes the insertion of the CHCO2Et group (from ethyl diazoacetate N2CHCO2Et, EDA) into the C–H bonds of methane, in a homogeneous process that uses supercritical carbon dioxide (scCO2) as the reaction medium. Other light alkanes such as ethane, propane, and butane have been also functionalized with this copper-based catalyst, in the first example of the derivatization of the series of C1–C4 alkanes with this metal and a soluble catalyst.

Childhood lead (Pb2+) intoxication is a public health problem of global proportion. Lead exposure during development produces multiple effects on the central nervous system including impaired synapse formation, altered synaptic plasticity, and learning deficits. In primary hippocampal neurons in culture and hippocampal slices, Pb2+ exposure inhibits vesicular release and reduces the number of fast-releasing sites, an effect associated with Pb2+ inhibition of NMDA receptor-mediated trans-synaptic Brain-Derived Neurotrophic Factor (BDNF) signaling. The objective of this study was to determine if activation of TrkB, the cognate receptor for BDNF, would rescue Pb2+-induced impairments of vesicular release. Rats were chronically exposed to Pb2+ prenatally and postnatally until 50 days of age. This chronic Pb2+ exposure paradigm enhanced paired-pulse facilitation of synaptic potentials in Schaffer collateral-CA1 synapses in the hippocampus, a phenomenon indicative of reduced vesicular release probability. Decreased vesicular release probability was confirmed by both mean-variance analysis and direct 2-photon imaging of vesicular release from hippocampal slices of rats exposed to Pb2+in vivo. We also found a Pb2+-induced impairment of calcium influx in Schaffer collateral-CA1 synaptic terminals. Intraperitoneal injections of Pb2+ rats with the TrkB receptor agonist 7,8-dihydroxyflavone (5 mg/kg) for 14-15 days starting at postnatal day 35, reversed all Pb2+-induced impairments of presynaptic transmitter release at Schaffer collateral-CA1 synapses. This study demonstrates for the first time that in vivo pharmacological activation of TrkB receptors by small molecules such as 7,8-dihydroxyflavone can reverse long-term effects of chronic Pb2+ exposure on presynaptic terminals, pointing to TrkB receptor activation as a promising therapeutic intervention in Pb2+-intoxicated children.

The first example of a diazo palladium adduct is reported. The complexes [(ArNHC−PPh)M(η-NC(Ph)COEt)] (M=Ni, 3; M=Pd, 4; ArNHC−PPh=3-(2,6-diisopropylphenyl)-1-[(diphenylphosphino)ethyl]imidazol-2-ylidene) were prepared by ligand exchange with styrene-coordinated precursors [(ArNHC−PPh)M(styrene)] (M=Ni, 1; M=Pd, 2). Complex 4 was fully characterized, including X-ray analyses; this constitutes the first example of a diazo adduct compound with palladium, thereby closing the gap between Groups 8 and 10 regarding this type of compounds., The authors wish to thank MINECO for financial support (CTQ2014‐52769‐C03‐01 and CTQ2011‐24502). S. G. R. thanks MINECO for a FPI fellowship.

Two families of nickel complexes bearing chelating diphenylphosphine-functionalized NHC ligands [NiII(ArNHCPPh2)(allyl)]Cl 1a (Ar = Mes); 1b, (Ar = 2,6-iPr2-C6H3) and [Ni0(ArNHCPPh2)(alkene)] 2a (Ar = 2,6-iPr2-C6H3, alkene = styrene); 2b (Ar = 2,6-iPr2-C6H3, alkene = diethyl fumarate) have been prepared and fully characterized. VT-NMR experiments in solution reveal that the allyl derivatives 1a–b are stereochemically nonrigid. The solid-state structure of the Ni0 derivative 2b is also reported. These complexes display interesting catalytic properties in various cross-coupling reactions. The precatalyst [Ni0(ArNHCPPh2)(styrene)] 2a was found to be the most active system. The bulkiness of the N-substituent on the imidazole ring and the low oxidation state of the metal center in 2a accounted for its enhanced catalytic performance. This system catalyzed effectively the coupling of (hetero)aryl chlorides with a range of nucleophiles including Grignard reagents, boronic acids, secondary amines and indoles.

International audience; The reaction of esters with ethyl diazoacetate catalyzed by the complex [F-27-Tp(4 Bo, 3CF2CF3)Ag(acetone)] generates alpha-(acyloxy)acetates in moderate to high yields. This is a novel transformation in the context of carbene-transfer reactions from diazo compounds that, according to experimental and theoretical data, is suggested to occur through zwitterionic intermediates.

The phototransformation of benzimidazole (BZ) and of the benzimidazole pesticide thiabendazole (TBZ) was investigated in aqueous solution in the absence and presence of the supramolecular host cucurbit[8]uril (CB8). ESI-MS and NMR reveal that both compounds form stable 1 : 2 host-guest complexes with CB8 (BZ2@CB8, TBZ2@CB8). The phototransformation of free BZ leads to dehydrodimerization, while for TBZ the photoreactivity leads to BZ, benzimidazole-2-carboximide and 2-acetylbenzimidazole. Inside CB8, BZ undergoes photohydrolysis to form 2-aminoformanilide, while for TBZ2@CB8 additional photoproducts were observed which are pH dependent. At pH 1.2 photolysis of TBZ2@CB8 leads to new red-shifted photoproducts with extended π conjugation.

Air pollution exposures are linked to cognitive and olfaction deficits, oxidative stress, neuroinflammation and neurodegeneration including frontal hyperphosphorylated tau and diffuse amyloid plaques in Mexico City children and young adults. Mexico City residents are chronically exposed to fine particulate matter (PM(2.5)) concentrations (containing toxic combustion and industrial metals) above the annual standard (15 μg/m(3)) and to contaminated water and soil. Here, we sought to address the brain-region-specific effects of metals and key neuroinflammatory and DNA repair responses in two air pollution targets: frontal lobe and olfactory bulb from 12 controls vs. 47 Mexico City children and young adults average age 33.06±4.8 SE years. Inductively coupled plasma mass spectrometry (metal analysis) and real time PCR (for COX2, IL1β and DNA repair genes) in target tissues. Mexico City residents had higher concentrations of metals associated with PM: manganese (p=0.003), nickel and chromium (p=0.02) along with higher frontal COX2 mRNA (p=0.008) and IL1β (p=0.0002) and COX2 (p=0.005) olfactory bulb indicating neuroinflammation. Frontal metals correlated with olfactory bulb DNA repair genes and with frontal and hippocampal inflammatory genes. Frontal manganese, cobalt and selenium increased with age in exposed subjects. Together, these findings suggest PM-metal neurotoxicity causes brain damage in young urbanites, the olfactory bulb is a target of air pollution and participates in the neuroinflammatory response and since metal concentrations vary significantly in Mexico City urban sub-areas, place of residency has to be integrated with the risk for CNS detrimental effects particularly in children.

D. Ralet et al. -- 11 pags., 10 figs., 3 tabs., Background: In the neutron-rich A≈100 mass region, rapid shape changes as a function of nucleon number as well as coexistence of prolate, oblate, and triaxial shapes are predicted by various theoretical models. Lifetime measurements of excited levels in the molybdenum isotopes allow the determination of transitional quadrupole moments, which in turn provides structural information regarding the predicted shape change. Purpose: The present paper reports on the experimental setup, the method that allowed one to measure the lifetimes of excited states in even-even molybdenum isotopes from mass A=100 up to mass A=108, and the results that were obtained. Method: The isotopes of interest were populated by secondary knock-out reaction of neutron-rich nuclei separated and identified by the GSI fragment separator at relativistic beam energies and detected by the sensitive PreSPEC-AGATA experimental setup. The latter included the Lund-York-Cologne calorimeter for identification, tracking, and velocity measurement of ejectiles, and AGATA, an array of position sensitive segmented HPGe detectors, used to determine the interaction positions of the γ ray enabling a precise Doppler correction. The lifetimes were determined with a relativistic version of the Doppler-shift-attenuation method using the systematic shift of the energy after Doppler correction of a γ-ray transition with a known energy. This relativistic Doppler-shift-attenuation method allowed the determination of mean lifetimes from 2 to 250 ps. Results: Even-even molybdenum isotopes from mass A=100 to A=108 were studied. The decays of the low-lying states in the ground-state band were observed. In particular, two mean lifetimes were measured for the first time: τ=29.7-9.1+11.3 ps for the 4+ state of Mo108 and τ=3.2-0.7+0.7 ps for the 6+ state of Mo102. Conclusions: The reduced transition strengths B(E2), calculated from lifetimes measured in this experiment, compared to beyond-mean-field calculations, indicate a gradual shape transition in the chain of molybdenum isotopes when going from A=100 to A=108 with a maximum reached at N=64. The transition probabilities decrease for Mo108 which may be related to its well-pronounced triaxial shape indicated by the calculations., This work was supported by the BMBF under Grants No. 05P09RDFN4, No. 05P12RDFN8, and No. 05P12PKFNE and by the LOEWE center HIC for FAIR. Part of this work was supported by the P2IO excellence center. This work was also supported by the European Community FP7–Capacities, ENSAR Contract No. 262010, by the Swedish Research Council under Contracts No. 2010-147, No. 2010-3694, No. 2011-5253, No. 2011-6127, and No. 2014-5558, by the IN2P3- GSI No. 02-42 collaboration, by the Science and Technology Facilities Council (STFC) and by MINECO, Spain, under Grant No. FPA2014-57196-C5, and Generalitat Valenciana, Spain, under Grant No. PROMETEOII/2014/019

Exposure to the toxic metalloid arsenic is associated with diabetes and cancer and causes proteotoxicity and endoplasmic reticulum (ER) stress at the cellular level. Adaptive responses to ER stress are implicated in cancer and diabetes; thus, understanding mechanisms of arsenic-induced ER stress may offer insights into pathogenesis. Here, we identify genes required for arsenite-induced ER stress response in a genome-wide RNAi screen. Using an shRNA library targeting ∼20,000 human genes, together with an ER stress cell model, we performed flow cytometry-based cell sorting to isolate cells with defective response to arsenite. Our screen discovered several genes modulating arsenite-induced ER stress, including sodium-dependent neutral amino acid transporter, SNAT2. SNAT2 expression and activity are up-regulated by arsenite, in a manner dependent on activating transcription factor 4 (ATF4), an important mediator of the integrated stress response. Inhibition of SNAT2 expression or activity or deprivation of its primary substrate, glutamine, specifically suppressed ER stress induced by arsenite but not tunicamycin. Induction of SNAT2 is coincident with the activation of the nutrient-sensing mammalian target of rapamycin (mTOR) pathway, which is at least partially required for arsenite-induced ER stress. Importantly, inhibition of the SNAT2 or the System L transporter, LAT1, suppressed mTOR activation by arsenite, supporting a role for these transporters in modulating amino acid signaling. These findings reveal SNAT2 as an important and specific mediator of arsenic-induced ER stress, and suggest a role for aberrant mTOR activation in arsenic-related human diseases. Furthermore, this study demonstrates the utility of RNAi screens in elucidating cellular mechanisms of environmental toxins.

We have previously reported that lead (Pb(2+)) exposure results in both presynaptic and postsynaptic changes in developing neurons as a result of inhibition of the N-methyl-d-aspartate receptor (NMDAR). NMDAR inhibition by Pb(2+) during synaptogenesis disrupts downstream trans-synaptic signaling of brain-derived neurotrophic factor (BDNF) and exogenous addition of BDNF can recover the effects of Pb(2+) on both presynaptic protein expression and presynaptic vesicular release. NMDAR activity can modulate other trans-synaptic signaling pathways, such as nitric oxide (NO) signaling. Thus, it is possible that other trans-synaptic pathways in addition to BDNF signaling may be disrupted by Pb(2+) exposure. The current study investigated whether exogenous addition of NO could recover the presynaptic vesicular proteins lost as a result of Pb(2+) exposure during synaptogenesis, namely Synaptophysin (Syn) and Synaptobrevin (Syb). We observed that exogenous addition of NO during Pb(2+) exposure results in complete recovery of whole-cell Syn levels and partial recovery of Syn and Syb synaptic targeting in Pb(2+)-exposed neurons.

The Pd0 complexes [(NHC)PdLn] (NHC=N-heterocyclic carbene ligand; L=styrene for n=2 or PR3 for n=1) efficiently catalyse olefin cyclopropanation by using ethyl diazoacetate (EDA) as the carbene source with activities that improve on previously described catalytic systems based on this metal. Mechanistic studies have shown that all of these catalyst precursors deliver the same catalytic species in solution, that is, [(IPr)Pd(sty)], a 14e- unsaturated intermediate that further reacts with EDA to afford [(IPr)Pd(=CHCO2Et)(sty)], from which the cyclopropane is formed. © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim., We thank Prof. P. J. Pérez (Univ. Huelva) for helpful and constructive comments on these studies. We thank the Ministerio de Ciencia e Innovación (grants CTQ2008–00042BQU and CTQ2011–24502) and the Junta de Andalucía (Proyecto P07-FQM-02794) for financial support. CM thanks the MEC for a research fellowship

In the brain, translocator protein (18 kDa) (TSPO), previously called peripheral benzodiazepine receptor (PBR), is a glial protein that has been extensively used as a biomarker of brain injury and inflammation. However, the functional role of TSPO in glial cells is not well characterized. In this study, we show that the TSPO-specific ligands R-PK11195 (PK) and Ro5-4864 (Ro) increased microglia proliferation and phagocytosis with no effect on migration. Both ligands increased reactive oxygen species (ROS) production, and this effect may be mediated by NADPH-oxidase. PK and Ro also produced a small but detectable increase in IL-1β release. We also examined the effect of PK and Ro on the expression of pro-inflammatory genes and cytokine release in lipopolysaccharide (LPS) and adenosine triphosphate (ATP) activated microglia. PK or Ro had no effect on LPS-induced increase of pro-inflammatory genes, but they both decreased the ATP-induced increase of COX-2 gene expression. Ro, but not PK, enhanced the LPS-induced release of IL-1β. However, Ro decreased the ATP-induced release of IL-1β and TNF-α, and PK decreased the ATP-induced release of TNF-α. Exposure to Ro in the presence of LPS increased the number of apoptotic microglia, an effect that could be blocked by PK. These findings show that TSPO ligands modulate cellular functions consistent with microglia activation. Further, when microglia are activated, these ligands may have therapeutic potential by reducing the expression of pro-inflammatory genes and cytokine release. Finally, Ro-like ligands may be involved in the elimination of activated microglia via apoptosis.

Lead (Pb(2+)) exposure is known to affect presynaptic neurotransmitter release in both in vivo and cell culture models. However, the precise mechanism by which Pb(2+) impairs neurotransmitter release remains unknown. In the current study, we show that Pb(2+) exposure during synaptogenesis in cultured hippocampal neurons produces the loss of synaptophysin (Syn) and synaptobrevin (Syb), two proteins involved in vesicular release. Pb(2+) exposure also increased the number of presynaptic contact sites. However, many of these putative presynaptic contact sites lack Soluble NSF attachment protein receptor complex proteins involved in vesicular exocytosis. Analysis of vesicular release using FM 1-43 dye confirmed that Pb(2+) exposure impaired vesicular release and reduced the number of fast-releasing sites. Because Pb(2+) is a potent N-methyl-D-aspartate receptor (NMDAR) antagonist, we tested the hypothesis that NMDAR inhibition may be producing the presynaptic effects. We show that NMDAR inhibition by aminophosphonovaleric acid mimics the presynaptic effects of Pb(2+) exposure. NMDAR activity has been linked to the signaling of the transsynaptic neurotrophin brain-derived neurotrophic factor (BDNF), and we observed that both the cellular expression of proBDNF and release of BDNF were decreased during the same period of Pb(2+) exposure. Furthermore, exogenous addition of BDNF rescued the presynaptic effects of Pb(2+). We suggest that the presynaptic deficits resulting from Pb(2+) exposure during synaptogenesis are mediated by disruption of NMDAR-dependent BDNF signaling.

Copper homoscorpionate complexes TpxCu(I)(NCMe) efficiently catalyze the Atom Transfer Radical Polymerization (ATRP) of methacrylate (MMA) and other methacrylates at 50 °C in the absence of any red...

Background Silica nanoparticles (SiNPs) are being formulated for cellular imaging and for nonviral gene delivery in the central nervous system (CNS), but it is unclear what potential effects SiNPs can elicit once they enter the CNS. As the resident macrophages of the CNS, microglia are the cells most likely to respond to SiNP entry into the brain. Upon activation, they are capable of undergoing morphological and functional changes. Objective We examined the effects of SiNP exposure using primary rat microglia. Methods We observed microglial uptake of SiNPs using transmission electron and fluorescence confocal microscopy. Microglial functions, including phagocytosis, generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS), expression of proinflammatory genes, and cytokine release, were measured after SiNP exposure at different concentrations. Results Microglia are capable of avidly taking up SiNPs at all concentrations tested. These same concentrations did not elicit cytotoxicity or a change in phagocytic activity. SiNPs did increase the productions of both intracellular ROS and RNS. We also observed a significant decrease in tumor necrosis factor-α gene expression at all concentrations tested and a significant increase in COX-2 (cyclooxygenase-2) gene expression at the highest concentration of SiNPs. Analysis of cytokine release showed a detectable level of interleukin-1β. Conclusions This is the first study demonstrating the in vitro effects of SiNPs in primary microglia. Our findings suggest that very low levels of SiNPs are capable of altering microglial function. Increased ROS and RNS production, changes in proinflammatory genes, and cytokine release may not only adversely affect microglial function but also affect surrounding neurons.

A series of complexes of general formulae Tp x Cu have been employed as the catalyst for the styrene cyclopropanation reaction with ethyl diazoacetate, both under homogeneous and heterogeneous conditions. Several solid supports have been tested, with silica gel being the most convenient for this transformation. A comparison of the results obtained under both conditions has shown that the catalytic pocket is affected by the support.

The neurological sequelae of chronic Mn exposure include psychiatric, cognitive, and motor deficits, suggesting the potential involvement of multiple neurotransmitter systems and brain regions. Available evidence in rodents suggests that Mn causes dysregulation of glutamatergic and gamma-aminobutyric acidergic (GABAergic) neurotransmitter systems. However, this has never been studied comprehensively in the nonhuman primate brain. Cynomolgus macaques were given weekly i.v. injections of 3.3-5.0 mg Mn/kg, 5.0-6.7 mg Mn/kg, or 8.3-10.0 mg Mn/kg for 7-59 weeks. Total glutamate, glycine, and GABA concentrations were measured by high performance liquid chromatography (HPLC) with fluorescence detection in 13 brain areas in Mn-treated and control monkeys. Neurotransmitter concentrations did not change with chronic Mn exposure. Quantitative autoradiography of the N-methyl-D-aspartate receptor, the GABAa receptor, and glutamate transporters was used to assess their regional distribution. Each of these neurotransmitter receptors remained almost universally unchanged with Mn treatment. Immunohistochemical analysis of glutamine synthetase (GS) demonstrated a selective Mn-induced decrease in the globus pallidus, which could potentially alter synaptic and/or astrocytic levels of glutamate. This study shows that in nonhuman primates with previous documentation of Mn-induced brain pathology, the glutamatergic and GABAergic systems appear to be mostly unaffected by chronic Mn exposure with the exception of reduced GS expression in the globus pallidus.

The long-term consequences of chronic manganese (Mn) exposure on neurological health is a topic of great concern to occupationally-exposed workers and in populations exposed to moderate levels of Mn. We have performed a comprehensive assessment of Mn effects on dopamine (DA) synapse markers using positron emission tomography (PET) in the non-human primate brain. Young male Cynomolgus macaques were given weekly i.v. injections of 3.3-5.0 mg Mn/kg (n = 4), 5.0-6.7 mg Mn/kg (n = 5), or 8.3-10.0 mg Mn/kg (n = 3) for 7-59 weeks and received PET studies of various DA synapse markers before (baseline) and at one or two time points during the course of Mn exposure. We report that amphetamine-induced DA release measured by PET is markedly impaired in the striatum of Mn-exposed animals. The effect of Mn on DA release was present in the absence of changes in markers of dopamine terminal integrity determined in post-mortem brain tissue from the same animals. These findings provide compelling evidence that the effects of Mn on DA synapses in the striatum are mediated by inhibition of DA neurotransmission and are responsible for the motor deficits documented in these animals.

Background Exposure to excess levels of the essential trace element manganese produces cognitive, psychiatric, and motor abnormalities. The understanding of Mn neurotoxicology is heavily governed by pathologic and neurochemical observations derived from rodent studies that often employ acute Mn exposures. The comparatively sparse studies incorporating in vivo neuroimaging in nonhuman primates provide invaluable insights on the effects of Mn on brain chemistry. Objectives The purpose of this review is to discuss important aspects of Mn neurotoxicology and to synthesize recent findings from one of the largest cohorts of nonhuman primates used to study the neurologic effects of chronic Mn exposure. Discussion We reviewed our recent in vivo and ex vivo studies that have significantly advanced the understanding of Mn-induced neurotoxicity. In those studies, we administered weekly doses of 3.3–5.0 (n = 4), 5.0–6.7 (n = 5), or 8.3–10.0 mg Mn/kg (n = 3) for 7–59 weeks to cynomolgus macaque monkeys. Animals expressed subtle deficits in cognition and motor function and decreases in the N-acetylaspartate-to-creatine ratio in the parietal cortex measured by magnetic resonance spectroscopy reflective of neuronal dysfunction. Impaired striatal dopamine release measured by positron emission tomography was observed in the absence of changes in markers of dopamine neuron degeneration. Neuropathology indicated decreased glutamine synthetase expression in the globus pallidus with otherwise normal markers of glutamatergic and GABAergic neurotransmission. Increased amyloid beta (A4) precursor-like protein 1 gene expression with multiple markers of neurodegeneration and glial cell activation was observed in the frontal cortex. Conclusions These findings provide new information on mechanisms by which Mn affects behavior, neurotransmitter function, and neuropathology in nonhuman primates.

The beyond mean field approximation combined with the Gogny interaction is used to analyze the spherical to prolate deformed shape transition in the Neodymium isotopic chain. The vibrator as well as the rotor limits are nicely reproduced while the transitional region is only qualitatively described probably due to the lack of triaxial correlations in the calculations. Our results do not support the interpretation of $^{150}$Nd as a critical point nucleus and question the interpretation of shape changes as nuclear shape phase transitions., Comment: 12 pages, 9 figures, accepted in Phys. Lett. B

We used positron emission tomography (PET) to measure the earliest change in dopaminergic synapses and glial cell markers in a chronic, low-dose MPTP non-human primate model of Parkinson's disease (PD). In vivo levels of dopamine transporters (DAT), vesicular monoamine transporter-type 2 (VMAT2), amphetamine-induced dopamine release (AMPH-DAR), D2-dopamine receptors (D2R) and translocator protein 18 kDa (TSPO) were measured longitudinally in the striatum of MPTP-treated animals. We report an early (2 months) decrease (46%) of striatal VMAT2 in asymptomatic MPTP animals that preceded changes in DAT, D2R, and AMPH-DAR and was associated with increased TSPO levels indicative of a glial response. Subsequent PET studies showed progressive loss of all pre-synaptic dopamine markers in the striatum with expression of parkinsonism. However, glial cell activation did not track disease progression. These findings indicate that decreased VMAT2 is a key pathogenic event that precedes nigrostriatal dopamine neuron degeneration. The loss of VMAT2 may result from an association with alpha-synuclein aggregation induced by oxidative stress. Disruption of dopamine sequestration by reducing VMAT2 is an early pathogenic event in the dopamine neuron degeneration that occurs in the MPTP non-human primate model of PD. Genetic or environmental factors that decrease VMAT2 function may be important determinants of PD.

Humans exposed to excess levels of manganese (Mn 2+ ) express psychiatric problems and deficits in attention and learning and memory. However, there is a paucity of knowledge on molecular mechanisms by which Mn 2+ produces such effects. We now report that Mn 2+ is a potent inhibitor of [ 3 H]-MK-801 binding to the NMDA receptor channel in rat neuronal membrane preparations. The inhibition of [ 3 H]-MK-801 to the NMDA receptor channel by Mn 2+ was activity-dependent since Mn 2+ was a more potent inhibitor in the presence of the NMDA receptor co-agonists glutamate and glycine ( K i = 35.9 ± 3.1 μM) than in their absence ( K i = 157.1 ± 6.5 μM). We also show that Mn 2+ is a NMDA receptor channel blocker since its inhibition of [ 3 H]-MK-801 binding to the NMDA receptor channel is competitive in nature. That is, Mn 2+ significantly increased the affinity constant ( K d ) with no significant effect on the maximal number of [ 3 H]-MK-801 binding sites ( B max ). Under stimulating conditions, Mn 2+ was equipotent in inhibiting [ 3 H]-MK-801 binding to NMDA receptors expressed in neuronal membrane preparations from different brain regions. However, under basal, non-stimulated conditions, Mn 2+ was more potent in inhibiting NMDA receptors in the cerebellum than other brain regions. We have previously shown that chronic Mn 2+ exposure in non-human primates increases Cu 2+ , but not zinc or iron concentrations in the basal ganglia [Guilarte TR, Chen M-K, McGlothan JL, Verina T, Wong DF, Zhou Y, Alexander M, Rohde CA, Syversen T, Decamp E, Koser AJ, Fritz S, Gonczi H, Anderson DW, Schneider JS. Nigrostriatal dopamine system dysfunction and subtle motor deficits in manganese-exposed non-human primates. Exp Neurol 2006a;202:381–90]. Therefore, we also tested the inhibitory effects of Cu 2+ on [ 3 H]-MK-801 binding to the NMDA receptor channel. The data shows that Cu 2+ in the presence of glutamate and glycine is a more potent inhibitor of the NMDA receptor than Mn 2+ . Our findings suggest that the inhibitory effect of Mn 2+ and/or Cu 2+ on the NMDA receptor may produce a deficit in glutamatergic transmission in the brain of individuals exposed to excess levels of Mn 2+ and produce neurological dysfunction.

Thermal reactions between [RuCl2(diene)]n (diene = 2,5-norbornadiene, nbd; 1,5-cyclooctadiene, cod) with an excess of N,N,N',N'-tetramethylethylene diamine (tmeda) afforded derivatives [RuCl2(diene)(tmeda)] (diene = nbd, 1; cod, 2) as a mixture of cis and trans isomers. When thermolysis was performed under H2 mixtures of hydride species [RuCl(H)(diene)(tmeda)] (diene = nbd, 3; cod, 4) and the bis-tmeda adduct trans-[RuCl2(tmeda)2] (5) were obtained in different ratios depending upon the reaction conditions and reaction times. Heating polymeric Ru(II) precursors in toluene in the presence of a 5-fold excess of the bulkier N,N,N',N'-tetraethylethylene diamine (teeda) resulted in a rare diamine dealkylation process with formation of trans-[RuCl2(nbd)(Et2NCH2CH2NHEt)] (6) and trans-[RuCl2(cod)(EtHNCH2CH2NHEt)] (7) in high yields. The presence of N-H functionalities in the coordinated diamine ligands of 6 and 7 was unambiguously established by single-crystal X-ray diffraction studies. The dealkylation process of the teeda ligand seems to proceed intramolecularly as shown by solution NMR studies performed with the soluble Ru(II) precursors trans-[RuCl2(amine)2(diene)] (diene = nbd, amine = morpholine, 9; diene = cod, amine = Et2NH, 10). The above complexes [RuCl2(diene)(diamine)] have been tested as precatalysts in the hydrogenation of ketones both for transfer as well as direct hydrogenation, the latter route being the most effective.

A study of the variables that affect the insertion of the :CHCO2Et group (formed from ethyl diazocetate, EDA) into the C–H bonds of cyclohexane in the presence of a TpxCu complex as the catalyst (Tpx = trispyrazolylborate ligand) has demonstrated an anomalous effect of the catalyst loading. The use of low concentrations of catalyst produces an increase in the yield of the C–H activation product ethyl cyclohexaneacetate. This effect has also been found in the case of other less elaborated catalysts such as [BpBr3Cu] or [(bipy)2Cu][I]. (© Wiley-VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2007)

Cu(I) complexes containing trispyrazolylborate ligands efficiently catalyze the atom transfer radical addition (ATRA) of polyhalogenated alkanes to various olefins under mild conditions. The catalytic activity is enhanced when bulky and electron donating Tpx ligands are employed. Kinetic data have allowed the proposal of a mechanistic interpretation that includes a Cu(II) pentacoordinated species that regulates the catalytic cycle.