Effects of O-2 pressure on the oxidation of VOx/Pt(111)

National Basic Research Program of China (973 program) [2010CB732303, 2013CB933102]; Chinese Ministry of Education [309019]; National Natural Science Foundation of China [21033006, 21073149, 20923004, 21273178]; Program for Changjiang Scholars and Innovative Research Team in Universities [IRT1036]; PhD Programs Foundation of the Chinese Ministry of Education [20110121110010]Vanadium oxide (VOx) has been extensively used in many oxidation and selective oxidation reactions. In this study, VOx thin films were prepared in an ultra-high vacuum (UHV) chamber by evaporating V onto a Pt(111) surface followed by subsequent oxidation at 623 K in 1 x 10(-7) Torr O-2, and further oxidized in the 'high-pressure' reaction cell with 1 Torr O-2. The film quality and structure were investigated by high-resolution electron energy loss spectroscopy (HREELS), X-ray photoelectron spectroscopy (XPS), low energy electron diffraction (LEED), low energy ion scattering spectroscopy (LEIS), Auger electron spectroscopy (AES), and in situ infrared reflection absorption spectroscopy (IRAS). On the Pt(111) surface, VOx forms isolated O=VOx (x = 0-3) species, surface two-dimensional (2D) (2 x 2)-V2O3 domains, a bi-layer structure with a (3 root 3 x 6) arrangement, and a complicated tri-layer structure as the coverage increases from submonolayer to multilayer. Under the UHV conditions, the oxidation state of V is mainly +3 and the stability was found to be surface V2O3 > bi-layer V2O3 > tri-layer one. After exposing to 0.3-1 Torr O-2, VOx can be oxidized to higher oxidation states, mainly V2O5, as evidenced by the shifts of the core-level binding energies and presence of V=O. These results indicate that thorough oxidation of VOx requires sufficiently high O-2 pressure, and that vanadium-based catalysts may possess higher oxidation states under most reaction conditions in the presence of O-2

Lipid profiles in the cerebrospinal fluid of rats with 6-hydroxydopamine-induced lesions as a model of Parkinson’s disease

BackgroundParkinson’s disease (PD) is a progressive neurodegenerative disease with characteristic pathological abnormalities, including the loss of dopaminergic (DA) neurons, a dopamine-depleted striatum, and microglial activation. Lipid accumulation exhibits a close relationship with these pathologies in PD.MethodsHere, 6-hydroxydopamine (6-OHDA) was used to construct a rat model of PD, and the lipid profile in cerebrospinal fluid (CSF) obtained from model rats was analyzed using lipidomic approaches.ResultsEstablishment of this PD model was confirmed by apomorphine-induced rotation behaviors, loss of DA neurons, depletion of dopamine in the striatum, and microglial activation after 6-OHDA-induced lesion generation. Unsupervised and supervised methods were employed for lipid analysis. A total of 172 lipid species were identified in CSF and subsequently classified into 18 lipid families. Lipid families, including eicosanoids, triglyceride (TG), cholesterol ester (CE), and free fatty acid (FFA), and 11 lipid species exhibited significantly altered profiles 2 weeks after 6-OHDA administration, and significant changes in eicosanoids, TG, CE, CAR, and three lipid species were noted 5 weeks after 6-OHDA administration. During the period of 6-OHDA-induced lesion formation, the lipid families and species showed concentration fluctuations related to the recovery of behavior and nigrostriatal abnormalities. Correlation analysis showed that the levels of eicosanoids, CE, TG families, and TG (16:0_20:0_18:1) exhibited positive relationships with apomorphine-induced rotation behaviors and negative relationships with tyrosine hydroxylase (TH) expression in the midbrain.ConclusionThese results revealed that non-progressive nigrostriatal degeneration induced by 6-OHDA promotes the expression of an impairment-related lipidomic signature in CSF, and the level of eicosanoids, CE, TG families, and TG (16:0_20:0_18:1) in CSF may reveal pathological changes in the midbrain after 6-OHDA insult

Genomewide linkage scan in a multigeneration Caucasian pedigree identifies a novel locus for keratoconus on chromosome 5q14.3-q21.1

Purpose: Keratoconus is a corneal dystrophy with an incidence of 1 in 2000 and a leading cause for cornea transplantation in Western developed countries. Both clinical observations and segregation analyses suggest a major role for genes in its pathogenesis. It is genetically heterogenous, most commonly sporadic, but inherited patterns with recessive or dominant modes have also been reported. We studied a four-generation autosomaldominant pedigree to identify disease loci for keratoconus. Methods: A two-stage genome-wide scan was applied to 27 family members. First linkage analysis was performed with 343 microsatellite markers along the 22 autosomal chromosomes at Ϸ10 cM density. This was followed by fine mapping at Ϸ2 cM density, in regions suggestive of linkage. Multipoint linkage analysis was performed using GeneHunter2. Results: Evidence of suggestive linkage from the initial scan was observed at the 82 to 112 cM region of chromosome 5q14.1-q21.3 with a maximum lod score (LOD) of 3.48 (penetrance ϭ 0.5). Fine mapping by testing an additional 11 microsatellite markers at 1 to 3 cM intervals revealed a narrower and higher peak (99 -119 cM) with LOD 3.53. By analysis of the recombination of haplotypes, the putative locus of keratoconus was further narrowed to a 6 cM region (8

System harmonic impedance calculation based on partial least squares equivalent weight regression

To mitigate the impact of singular values in voltage and current signals on regression results and achieve a more accurate delineation of harmonic responsibilities for both the system and users， this paper proposes a method for calculating system harmonic impedance based on partial least squares （PLS） equivalent weight regression. Utilizing harmonic voltage and current data from common connection points， the paper formulates a regression equation containing the sought-after parameters. The PLS is then employed to determine regression coefficients， which correspond to the harmonic impedance and harmonic voltage on the system side. These coefficients are used as initial values for iterative equivalent weight calculations. Then， the user’s harmonic emission level is deduced based on the iterative results. This approach overcomes the drawbacks of using the least squares solution as an initial value for iterative calculations， enhancing the precision of user’s harmonic emission level calculations. The accuracy of the proposed method is validated through simulation analysis in case studies

Parkinson’s disease in a patient with GBA and LRRK2 covariants after acute hypoxic insult: a case report

Abstract Background The glucocerebrosidase (GBA) and leucine-rich repeat kinase 2 (LRRK2) genes are associated with the risk of sporadic Parkinson’s disease (PD). As an environmental factor, hypoxic insults may impair dopamine neurons in the substantia nigra and exacerbate PD symptoms. However, covariants of GBA and LRRK2 combined with hypoxic insults in clinical cases of Parkinsonism have not yet been reported. Case presentation A 69-year-old male patient with PD and his relatives were clinically characterized and sequenced using the whole-exome technique. A novel covariant, c.1448 T > C (p. L483P, rs421016) on GBA and c.691 T > C (p. S231P, rs201332859) on LRRK2 were identified in this patient who first developed bradykinesia and rigidity in the neck at one month after an acute hypoxic insult during mountaineering. The patient presented with a mask-like face, festinating gait, asymmetric bradykinesia, and moderate rigidity. These symptoms were treated with levodopa and pramipexole, resulting in a 65% improvement in the Unified Parkinson’s Disease Rating Scale (UPDRS) motor score. These parkinsonian symptoms persisted and developed with hallucinations, constipation, and rapid eye movement sleep behavior disorder. After 4 years, the patient exhibited a wearing-off phenomenon and died from pulmonary infection 8 years after disease onset. His parents, wife, and siblings were not diagnosed with PD, and his son carried p. L483P without Parkinsonism-like symptoms. Conclusions This is a case report of PD after hypoxic insult in a patient carrying a covariant of GBA and LRRK2. This study may help us understand the interaction between genetic and environmental factors in clinical PD

Micro-Change Process of Calcium–Magnesium Double Expansive Agent and Its Performance Characterization in Cement-Based Materials

With the increase of cement output, the demand for cement expansion agents increases, and composite expansion agents have become the development trend. The purpose of this study is to study the microscopic change process and expansion effect of calcium oxide and magnesium oxide double expansion agents. After calcination at different temperatures, the change process of microscopic morphology of calcined products was observed. Through calcining dolomite at 900 °C, the mixture D900 of calcium oxide and magnesium oxide was obtained. To prepare mixed cement, 10 wt %, 20 wt %, and 30 wt % of D900 were added into cement to prepare mixed cement. At the same time, the compressive strength, deformation, and porosity of mixed cement were measured. The results show that adding D900 improves the expansion rate of early cement paste and reduces the compressive strength. After 120 days, the compressive strength of 20 wt % cement paste is higher than that of blank cement paste, and the porosity of 20 wt % cement paste is the lowest among the three mixed cements. This shows that 20 wt % is a more suitable substitute

A case of congenital afibrinogenemia with multiple thrombotic and hemorrhagic disorders

Abstract This is a case of congenital afibrinogenemia with multiple thrombotic and hemorrhagic events. His fibrinogen concentration was negatively correlated with thrombin time and prothrombin time and abnormally negatively correlated with plasma D‐dimer levels. The individualized standard for fibrinogen concentration may help to balance thrombotic and hemorrhagic events for this disease

Effect of Hydration Temperature Rise Inhibitor on the Temperature Rise of Concrete and Its Mechanism

The rapid drop in internal temperature of mass concrete can readily lead to temperature cracks. Hydration heat inhibitors reduce the risk of concrete cracking by reducing the temperature during the hydration heating phase of cement-based material but may reduce the early strength of the cement-based material. Therefore, in this paper, the influence of commercially available hydration temperature rise inhibitors on concrete temperature rise is studied from the aspects of macroscopic performance and microstructure characteristics, and their mechanism of action is analyzed. A fixed mix ratio of 64% cement, 20% fly ash, 8% mineral powder and 8% magnesium oxide was used. The variable was different admixtures of hydration temperature rise inhibitors at 0%, 0.5%, 1.0% and 1.5% of the total cement-based materials. The results showed that the hydration temperature rise inhibitors significantly reduced the early compressive strength of concrete at 3 d, and the greater the amount of hydration temperature rise inhibitors, the more obvious the decrease in concrete strength. With the increase in age, the influence of hydration temperature rise inhibitor on the compressive strength of concrete gradually decreased, and the decrease in compressive strength at 7 d was less than that at 3 d. At 28 d, the compressive strength of the hydration temperature rise inhibitor was about 90% in the blank group. XRD and TG confirmed that hydration temperature rise inhibitors delay early hydration of cement. SEM showed that hydration temperature rise inhibitors delayed the hydration of Mg(OH)2