Architecture of industrial Bi-Mo-Co-Fe-K-O propene oxidation catalysts.

Industrial heterogeneous catalysts show high performance coupled with high material complexity. Deconvoluting this complexity into simplified models eases mechanistic studies. However, this approach dilutes the relevance because models are often less performing. We present a holistic approach to reveal the origin of high performance without losing the relevance by pivoting the system at an industrial benchmark. Combining kinetic and structural analyses, we show how the performance of Bi-Mo-Co-Fe-K-O industrial acrolein catalysts occurs. The surface BiMoO ensembles decorated with K supported on ß-Co1-xFexMoO4 perform the propene oxidation, while the K-doped iron molybdate pools electrons to activate dioxygen. The nanostructured vacancy-rich and self-doped bulk phases ensure the charge transport between the two active sites. The features particular to the real system enable the high performance.

Oxidation Catalysis over Solid-State Keggin-Type Phosphomolybdic Acid with Oxygen Defects.

Keggin-type phosphomolybdic acid (PMo12O40), treated with pyridine (Py), forms a crystalline material (PyPMo-HT) following heat treatment under an inert gas flow at ∼420 °C. Although this material is known to have attractive catalytic properties for gas-phase oxidation, the origin of this catalytic activity requires clarification. In this study, we investigated the crystal structure of PyPMo-HT. PyPMo-HT comprises a one-dimensional array of Keggin units and pyridinium cations (HPy), with an HPy/Keggin unit ratio of ∼1.0. Two oxygen atoms were removed from the Keggin unit during crystal structure transformation, which resulted in an electron being localized on the Mo atom in close contact with the adjacent Keggin unit. Upon the introduction of molecular oxygen, electron transfer from this Mo atom resulted in the formation of an electrophilic oxygen species that bridged two Keggin units. The electrophilic oxygen species acted as a catalytically active oxygen species, as confirmed by the selective oxidation of propylene. PyPMo-HT showed excellent catalytic activity for the selective oxidation of methacrolein, with the methacrylic acid yield being superior to that obtained with PMo12O40 and comparable to that obtained with an industrial Keggin-type polyoxometalate (POM) catalyst. The oxidation catalysis observed over PyPMo-HT provides a deeper understanding of POM-based industrial catalytic processes.

Dynamics of palladium on nanocarbon in the direct synthesis of H2O2.

This work aims to clarify the nanostructural transformation accompanying the loss of activity and selectivity for the hydrogen peroxide synthesis of palladium and gold-palladium nanoparticles supported on N-functionalized carbon nanotubes. High-resolution X-ray photoemission spectroscopy (XPS) allows the discrimination of metallic palladium, electronically modified metallic palladium hosting impurities, and cationic palladium. This is paralleled by the morphological heterogeneity observed by high-resolution TEM, in which nanoparticles with an average size of 2 nm coexisted with very small palladium clusters. The morphological distribution of palladium is modified after reaction through sintering and dissolution/redeposition pathways. The loss of selectivity is correlated to the extent to which these processes occur as a result of the instability of the particle at the carbon surface. We assign beneficial activity in the selective hydrogenation of oxygen to palladium clusters with a modified electronic structure compared with palladium metal or palladium oxides. These beneficial species are formed and stabilized on carbons modified with nitrogen atoms in substitutional positions. The formation of larger metallic palladium particles not only reduces the number of active sites for the synthesis, but also enhances the activity for deep hydrogenation to water. The structural instability of the active species is thus detrimental in a dual way. Minimizing the chance of sintering of palladium clusters by all means is thus the key to better performing catalysts.

How strain affects the reactivity of surface metal oxide catalysts.

Highly dispersed molybdenum oxide supported on mesoporous silica SBA-15 has been prepared by anion exchange resulting in a series of catalysts with changing Mo densities (0.2-2.5 Mo atoms nm(-2) ). X-ray absorption, UV/Vis, Raman, and IR spectroscopy indicate that doubly anchored tetrahedral dioxo MoO4 units are the major surface species at all loadings. Higher reducibility at loadings close to the monolayer measured by temperature-programmed reduction and a steep increase in the catalytic activity observed in metathesis of propene and oxidative dehydrogenation of propane at 8 % of Mo loading are attributed to frustration of Mo oxide surface species and lateral interactions. Based on DFT calculations, NEXAFS spectra at the O-K-edge at high Mo loadings are explained by distorted MoO4 complexes. Limited availability of anchor silanol groups at high loadings forces the MoO4 groups to form more strained configurations. The occurrence of strain is linked to the increase in reactivity.

In situ generation of active sites in olefin metathesis.

The depth of our understanding in catalysis is governed by the information we have about the number of active sites and their molecular structure. The nature of an active center on the surface of a working heterogeneous catalyst is, however, extremely difficult to identify and precise quantification of active species is generally missing. In metathesis of propene over dispersed molybdenum oxide supported on silica, only 1.5% of all Mo atoms in the catalyst are captured to form the active centers. Here we combine infrared spectroscopy in operando with microcalorimetry and reactivity studies using isotopic labeling to monitor catalyst formation. We show that the active Mo(VI)-alkylidene moieties are generated in situ by surface reaction of grafted molybdenum oxide precursor species with the substrate molecule itself gaining insight into the pathways limiting the number of active centers on the surface of a heterogeneous catalyst. The active site formation involves sequential steps requiring multiple catalyst functions: protonation of propene to surface Mo(VI)-isopropoxide species driven by surface Brønsted acid sites, subsequent oxidation of isopropoxide to acetone in the adsorbed state owing to the red-ox capability of molybdenum leaving naked Mo(IV) sites after desorption of acetone, and oxidative addition of another propene molecule yielding finally the active Mo(VI)-alkylidene species. This view is quite different from the one-step mechanism, which has been accepted in the community for three decades, however, fully consistent with the empirically recognized importance of acidity, reducibility, and strict dehydration of the catalyst. The knowledge acquired in the present work has been successfully implemented for catalyst improvement. Simple heat treatment after the initial propene adsorption doubled the catalytic activity by accelerating the oxidation and desorption-capturing steps, demonstrating the merit of knowledge-based strategies in heterogeneous catalysis. Molecular structure of active Mo(VI)-alkylidene sites derived from surface molybdena is discussed in the context of similarity to the highly active Schrock-type homogeneous catalysts.

Sustained exogenous administration of Met5-enkephalin protects against infarction in vivo.

The opioid antagonist naloxone abolishes infarct limitation by myocardial ischemic preconditioning, suggesting that one or more endogenous opioid peptides can mediate cardiac protection against ischemic damage. We tested the hypothesis that the naturally occurring opioid peptide Met5-enkephalin (ME) modulates myocardial infarct size in vivo. Experiments were conducted in barbiturate-anesthetized open-chest rabbits subjected to regional myocardial ischemia-reperfusion. ME was administered via osmotic minipump for 24 h. Infarct size was assessed with tetrazolium and is expressed as a percentage of the area at risk. Exogenous ME reduced the amount of the risk zone infarcted by approximately 60% compared with saline-treated controls. ME-induced protection was sensitive to opioid receptor blockade with naloxone [NAL 50 +/- 2% vs. ME + NAL 39 +/- 3%, P = not significant (NS)] and also to blockade of sarcolemmal and mitochondrial ATP-sensitive K+ (KATP) channels [5-hydroxydecanoate (5-HD) 33 +/- 3% vs. ME + 5-HD 43 +/- 8%, P = NS; and HMR-1098 60 +/- 3% vs. ME + HMR-1098 54 +/- 7%, P = NS]. We conclude that ME limits ischemic injury in vivo by an opioid receptor-mediated mechanism that involves both sarcolemmal and mitochondrial KATP channels.

Percutaneous cervical cordotomy and subarachnoid phenol block using fluoroscopy in pain control of costopleural syndrome.

We examined the efficacy of percutaneous cervical cordotomy (PCC) and subarachnoid phenol block using fluoroscopy (SAPB-F) for control of chest and/or back pain from costopleural syndrome. The efficacy of each block was evaluated by changes in pain score (PS), analgesic dose and performance status 1 week after the block, as well as by the complications. Between 1980 and 1986, PCC was performed in 10 patients. SAPB-F was performed in 13 patients between 1987 and 1991. Pain was not well controlled by analgesics in any of these patients. For PCC the follow-up period was 94.7 +/- 71.1 days. PS (VAS, 0-10) reduced from 8.5 +/- 0.9 to 3.0 +/- 2.7. No analgesics were needed in 4 patients. Pain recurred in 1 patient. Hemiparesis occurred in 2 patients. General fatigue occurred in 6 patients. In 4 patients with these complications performance status deteriorated and did not recover during the follow-up period. For SAPB-F the follow-up period was 71.8 +/- 44.0 days. SAPB-F was designed to achieve selective phenol deposit at the targeted nerve root. PS decreased from 7.5 +/- 1.9 to 2.7 +/- 2.6. No analgesics were needed in 5 patients. Pain recurred in 3 patients. There were no complications and no changes in performance status. From this study we concluded that PCC is an effective method of pain control for costopleural syndrome, but a risk of serious complications is involved. SAPB-F is an effective and safe method and should be the first choice of nociceptive pathway block.

Ipsilateral referral of pain following cordotomy.

We report a patient who developed ipsilateral referred pain following unilateral percutaneous cervical cordotomy (PCC). A right-sided PCC was performed on a 44-year-old woman who had been suffering from left groin and thigh pain caused by a fibrosarcoma. PCC produced analgesia below T7 on the left side, and the pain disappeared. A novel spontaneous pain with prominent allodynia occurred postoperatively in the right infraclavicular region (C3-C4). Strong pressure on the left groin where severe spontaneous pain and tenderness had been before PCC increased the new pain, and an epidural block which produced analgesia below T10 relieved the new pain. These facts indicate that the new pain was induced by afferent inputs from the originally painful region.

Reference of pain following percutaneous cervical cordotomy.

In order to clarify the mechanism of reference of pain following cordotomy (ROPC), the authors investigated ROPC in 66 patients undergoing percutaneous cervical cordotomy (PCC) and examined the features of ROPC and the correlation between the occurrence of ROPC and the pre-operative pain states, as well as the results of PCC. ROPC was observed in 7 patients. It occurred immediately after PCC in 6 of 7 patients and 6 h after PCC in 1 patient. The pain was referred horizontally and cranially from the region rendered totally or largely analgesic by PCC to the normally innervated region. The region to which the pain was referred was not fixed. The referred pain disappeared by rendering the region where referred pain was felt analgesic with additional PCC. There was no correlation between the occurrence of ROPC and pre-operative pain states, or the results of PCC. From these results we postulate that: (1) ROPC occurs via a subsidiary pathway consisting of ascending chains of short neurons connecting dorsal horn neurons longitudinally and latitudinally; (2) the subsidiary pathway is inhibited under normal conditions by feedback inhibition from second-order neurons and/or higher central neurons of the nociceptive pathway; and (3) ROPC results from the release of the feedback inhibition by cordotomy.