Paramagnetic NMR of Phenolic Oxime Copper Complexes: A Joint Experimental and Density Functional Study.

1 H and 13 C pNMR properties of bis(salicylaldoximato)copper(II) were studied in the solid state using magic-angle-spinning NMR spectroscopy and, for the isolated complex and selected oligomers, using density-functional theory at the PBE0-1/3 //PBE0-D3 level. Large paramagnetic shifts are observed, up to δ(1 H)=272 ppm and δ(13 C)=1006 ppm (at 298 K), which are rationalised through spin delocalisation from the metal onto the organic ligand and the resulting contact shifts arising from hyperfine coupling. The observed shift ranges are best reproduced computationally using exchange-correlation functionals with a high fraction of exact exchange (such as PBE0-1/3 ). Through a combination of experimental techniques and first-principles computation, a near-complete assignment of the observed signals is possible. Intermolecular effects on the pNMR shifts, modelled computationally in the dimers and trimers through effective decoupling between the local spins via A-tensor and total spin rescaling in the pNMR expression, are indicated to be small. Addition of electron-donating substituents and benzannelation of the organic ligand is predicted computationally to induce notable changes in the NMR signal pattern, which suggests that pNMR spectroscopy can be a sensitive probe for the spin distribution in paramagnetic phenolic oxime copper complexes.

Backbone-functionalised ruthenium diphosphine complexes for catalytic upgrading of ethanol and methanol to iso-butanol.

Efficient catalysts for Guerbet-type ethanol/methanol upgrading to iso-butanol have been developed via Michael addition of a variety of amines to ruthenium-coordinated dppen (1,1-bis(diphenylphosphino)ethylene). All catalysts produce over 50% iso-butanol yield with >90% selectivity in 2 h with catalyst 1 showing the best activity (74% yield after this time). The selectivity and turnover number approach 100% and 1000 respectively using catalyst 6. The presence of uncoordinated functionalised donor groups in these complexes results in a more stable catalyst compared to unfunctionalised analogues.

Calculation and experimental measurement of paramagnetic NMR parameters of phenolic oximate Cu(ii) complexes.

We present a strategy for predicting the unusual 1H and 13C shifts in NMR spectra of paramagnetic bisoximato copper(ii) complexes using DFT. We demonstrate good agreement with experimental measurements, although 1H-13C correlation spectra show that a combined experimental and theoretical approach remains necessary for full assignment.

'Preconditioning' with low dose lipopolysaccharide aggravates the organ injury / dysfunction caused by hemorrhagic shock in rats.

METHODS: Male rats were 'pretreated' with phosphate-buffered saline (PBS; i.p.) or LPS (1 mg/kg; i.p.) 24 h prior to HS. Mean arterial pressure (MAP) was maintained at 30 ± 2 mmHg for 90 min or until 25% of the shed blood had to be re-injected to sustain MAP. This was followed by resuscitation with the remaining shed blood. Four hours after resuscitation, parameters of organ dysfunction and systemic inflammation were assessed. RESULTS: HS resulted in renal dysfunction, and liver and muscular injury. At a first glance, LPS preconditioning attenuated organ dysfunction. However, we discovered that HS-rats that had been preconditioned with LPS (a) were not able to sustain a MAP at 30 mmHg for more than 50 min and (b) the volume of blood withdrawn in these animals was significantly less than in the PBS-control group. This effect was associated with an enhanced formation of the nitric oxide (NO) derived from inducible NO synthase (iNOS). Thus, a further control group in which all animals were resuscitated after 50 min of hemorrhage was performed. Then, LPS preconditioning aggravated both circulatory failure and organ dysfunction. Most notably, HS-rats pretreated with LPS exhibited a dramatic increase in NF-κB activation and pro-inflammatory cytokines. CONCLUSION: In conclusion, LPS preconditioning predisposed animals to an earlier vascular decompensation, which may be mediated by an excess of NO production secondary to induction of iNOS and activation of NF-κB. Moreover, LPS preconditioning increased the formation of pro-inflammatory cytokines, which is likely to have contributed to the observed aggravation of organ injury/dysfunction caused by HS.