A study of the reactivity of reduced molybdenum ethoxides: Synthesis and characterization of MoO(OH) and some novel molybdenum ethoxide cluster molecules

A low temperature route was used in an attempt to produce reduced molybdenum oxides. When molybdenum (III) ethoxide was hydrolyzed with the stoichiometric amount of water in hydrocarbon solvent, a quantitative yield of product was recovered. Elemental and molybdenum oxidation state analyses on this material indicated an empirical formula of Mo[subscript]2(OH)[subscript]5(OEt). When this material was heated in the presence of hydrogen at 250°C, a black solid was produced. Analyses indicated the material is MoO(OH). All attempts to thermally decompose MoO(OH) to the oxide, Mo[subscript]2O[subscript]3, were unsuccessful. A mixture of Mo[subscript]2O[subscript]3 and MoO[subscript]2 was produced instead. However, MoO(OH) was used, successfully, to synthesize LiMoO[subscript]2 from a reaction with Li[subscript]2CO[subscript]3 at 600°C. In addition, MoO(OH) was also used to synthesize Na[subscript] xMoO[subscript]2 (where x = 0.66);In an attempt to remove the final ethoxide ligand of Mo[subscript]2(OH)[subscript]5(OEt) by reaction with water to produce the pure hydroxide species, Mo(OH)[subscript]3, the hydrolysis reaction was completed using an excess (2-4 molar excess) of water. The solid recovered from this reaction still retained the ethoxide ligand and was slightly oxidized by the excess water. Surprisingly, however, the filtrate of the reaction afforded crystals with the formula, Mo[subscript]6O(OEt)[subscript]18 · 4.8H[subscript]2O. The yield of Mo[subscript]6O(OEt)[subscript]18 was very small. Therefore, attempts were made to synthesize it from reactions of Mo(OEt)[subscript]3 with other oxidizing agents, such as Sb[subscript]2O[subscript]5, C[subscript]6H[subscript]5IO, (CH[subscript]3)[subscript]3NO, and N[subscript]2O. However, these reactions did not successfully produce the cluster;Finally, an alternate synthetic route to isolate reduced molybdenum ethoxides was explored. Mo[subscript]2Cl[subscript]4py[subscript]4 was used in a reaction with sodium ethoxide in neat ethanol. When the reaction was carried out at room temperature overnight, a brown crystalline material was isolated from the ethanol. Elemental analysis of this material suggested the empirical formula could be written as Mo[subscript]4(OEt)[subscript]10py. Single crystal x-ray analysis was not completed due to the highly twinned nature of these crystals;When this reaction was completed in refluxing ethanol, a mixture of homoleptic molybdenum ethoxide species was isolated. Furthermore, a reaction of this molybdenum ethoxide mixture with iodosobenzene produced the novel cluster, Mo[subscript]4(OEt)[subscript]14(HOEt)[subscript]2

Frontally mediated inhibitory processing and white matter microstructure: age and alcoholism effects

RationaleThe NOGO P3 event-related potential is a sensitive marker of alcoholism, relates to EEG oscillation in the δ and θ frequency ranges, and reflects activation of an inhibitory processing network. Degradation of white matter tracts related to age or alcoholism should negatively affect the oscillatory activity within the network.ObjectiveThis study aims to evaluate the effect of alcoholism and age on δ and θ oscillations and the relationship between these oscillations and measures of white matter microstructural integrity.MethodsData from ten long-term alcoholics to 25 nonalcoholic controls were used to derive P3 from Fz, Cz, and Pz using a visual GO/NOGO protocol. Total power and across trial phase synchrony measures were calculated for δ and θ frequencies. DTI, 1.5 T, data formed the basis of quantitative fiber tracking in the left and right cingulate bundles and the genu and splenium of the corpus callosum. Fractional anisotropy and diffusivity (λL and λT) measures were calculated from each tract.ResultsNOGO P3 amplitude and δ power at Cz were smaller in alcoholics than controls. Lower δ total power was related to higher λT in the left and right cingulate bundles. GO P3 amplitude was lower and GO P3 latency was longer with advancing age, but none of the time-frequency analysis measures displayed significant age or diagnosis effects.ConclusionsThe relation of δ total power at CZ with λT in the cingulate bundles provides correlational evidence for a functional role of fronto-parietal white matter tracts in inhibitory processing

Role of N-Methyl-D-Aspartate Receptors in Action-Based Predictive Coding Deficits in Schizophrenia

BACKGROUND: Recent theoretical models of schizophrenia posit that dysfunction of the neural mechanisms subserving predictive coding contributes to symptoms and cognitive deficits, and this dysfunction is further posited to result from N-Methyl D-aspartate glutamate receptor (NMDAR) hypofunction. Previously, by examining auditory cortical responses to self-generated speech sounds, we demonstrated that predictive coding during vocalization is disrupted in schizophrenia. In order to test the hypothesized contribution of NMDAR hypofunction to this disruption, we examined the effects of the NMDAR antagonist, ketamine, on predictive coding during vocalization in healthy volunteers and compared them to the effects of schizophrenia. METHODS: In two separate studies, the N1 component of the event-related potential (ERP) elicited by speech sounds during vocalization (Talk) and passive playback (Listen) were compared to assess the degree of N1 suppression during vocalization, a putative measure of auditory predictive coding. In the cross-over study, 31 healthy volunteers completed two randomly ordered test days, a saline day and a ketamine day. ERPs during the Talk/Listen task were obtained pre-infusion and during infusion on both days, and N1 amplitudes were compared across days. In the case-control study, N1 amplitudes from 34 schizophrenia patients and 33 healthy controls were compared. RESULTS: N1 suppression to self-produced vocalizations was significantly and similarly diminished by ketamine (Cohen's d=1.14) and schizophrenia (Cohen's d=.85). CONCLUSIONS: Disruption of NMDARs causes dysfunction in predictive coding during vocalization in a manner similar to the dysfunction observed in schizophrenia patients, consistent with the theorized contribution of NMDAR hypofunction to predictive coding deficits in schizophrenia

Relating Intrinsic Low-Frequency BOLD Cortical Oscillations to Cognition in Schizophrenia

The amplitude of low-frequency fluctuations (ALFF) in the blood oxygenation level-dependent (BOLD) signal during resting-state fMRI reflects the magnitude of local low-frequency BOLD oscillations, rather than interregional connectivity. ALFF is of interest to studies of cognition because fluctuations in spontaneous intrinsic brain activity relate to, and possibly even constrain, task-evoked brain responses in healthy people. Lower ALFF has been reported in schizophrenia, but the cognitive correlates of these reductions remain unknown. Here, we assess relationships between ALFF and attention and working memory in order to establish the functional relevance of intrinsic BOLD oscillatory power alterations with respect to specific cognitive impairments in schizophrenia. As part of the multisite FBIRN study, resting-state fMRI data were collected from schizophrenia subjects (SZ; n=168) and healthy controls (HC; n=166). Voxelwise fractional ALFF (fALFF), a normalized ALFF measure, was regressed on neuropsychological measures of sustained attention and working memory in SZ and HC to identify regions showing either common slopes across groups or slope differences between groups (all findings p<0.01 height, p<0.05 family-wise error cluster corrected). Poorer sustained attention was associated with smaller fALFF in the left superior frontal cortex and bilateral temporoparietal junction in both groups, with additional relationships in bilateral posterior parietal, posterior cingulate, dorsal anterior cingulate (ACC), and right dorsolateral prefrontal cortex (DLPFC) evident only in SZ. Poorer working memory was associated with smaller fALFF in bilateral ACC/mPFC, DLPFC, and posterior parietal cortex in both groups. Our findings indicate that smaller amplitudes of low-frequency BOLD oscillations during rest, measured by fALFF, were significantly associated with poorer cognitive performance, sometimes similarly in both groups and sometimes only in SZ, in regions known to subserve sustained attention and working memory. Taken together, these data suggest that the magnitude of resting-state BOLD oscillations shows promise as a biomarker of cognitive function in health and disease