Explore the vast range of titles available.

Mn-based oxides are promising for the selective catalytic reduction (SCR) of NOx with NH 3 at temperatures below 200 °C. There is a general agreement that combining Mn with another metal oxide, such as CeOx improves catalytic activity. However, to date, there is an unsettling debate on the effect of Ce. To solve this, here we have systematically investigated a large number of catalysts. Our results show that, at low-temperature, the intrinsic SCR activity of the Mn active sites is not positively affected by Ce species in intimate contact. To confirm our findings, activities reported in literature were surface-area normalized and the analysis do not support an increase in activity by Ce addition. Therefore, we can unequivocally conclude that the beneficial effect of Ce is textural. Besides, addition of Ce suppresses second-step oxidation reactions and thus N 2 O formation by structurally diluting MnOx. Therefore, Ce is still an interesting catalyst additive. The role of Ce one Mn-based catalysts for the selective catalytic reduction of NOx at low temperature is an ongoing debate. Here the authors demonstrate that Ce has a structural promoting effect but impacts negatively on the intrinsic catalytic activity of Mn.

Cognitive and visual impairment are common in Huntington’s Disease (HD) and may precede motor diagnosis. We investigate the early presence of visual cognitive deficits in 181 participants, including HD carriers (40 pre-manifest, 30 early manifest, 27 manifest, and 6 reduced penetrance) and 78 healthy controls (HC). Significant differences in visual memory were observed between reduced penetrance and pre-manifest groups ( p  = .003), with pre-manifest showing worse performance. Age, education, CAG repeats, motor status, executive function, and verbal fluency, accounted for up to 72.8% of the variance in general and visual cognitive functions, with motor status having the strongest impact on visual domains in HD carriers. In pre-manifest HD, visual cognitive domains were primarily influenced by executive function, verbal fluency, age, and CAG repeats, while in early and manifest stages motor status and verbal fluency becomes more influential. ROC analyses showed that especially visuospatial abilities, visual memory, and visual attention (AUC = 0.927, 0.878, 0.874, respectively) effectively differentiated HC and pre-manifest from early and manifest HD. Early assessment of visual cognitive domains, particularly visual memory, could be an early marker of cognitive decline in HD. Our findings highlight the different profiles of impairment in visual cognition across HD carriers.

Wet-kneaded silica–magnesia is a benchmark catalyst for the one-step ethanol-to-butadiene Lebedev process. Magnesium silicates, formed during wet kneading, have been proposed as the active sites for butadiene formation, and their properties are mainly explained in terms of the ratio of acid and base sites. However, their mechanism of formation and reactivity have not yet been fully established. Here we show that magnesium silicates are formed by the dissolution of Si and Mg subunits from their precursors, initiated by the alkaline pH of the wet-kneading medium, followed by cross-deposition on the precursor surfaces. Using two individual model systems (Mg/SiO 2 and Si/MgO), we demonstrate that the location of the magnesium silicates (that is, Mg on SiO 2 or Si on MgO) governs not only their chemical nature, but also the configuration of adsorbed ethanol and resulting selectivity. By using an NMR approach together with probe molecules, we demonstrate that acid and basic sites in close atomic proximity (~5 Å) promote butadiene formation. The Lebedev process is an established approach to convert ethanol into butadiene catalysed by silica–magnesia prepared by the so-called wet-kneading method. However, the role and impact of this wet-kneading approach have not been fully uncovered. Here the authors reveal important aspects of this process and elucidate the role of the different active sites it generates within silica–magnesia.

Elevated urine bis(monoacylglycerol)phosphate (BMP) levels have been found in gain-of-kinase function LRRK2 G2019S mutation carriers. Here, we have expanded urine BMP analysis to other Parkinson’s disease (PD) associated mutations and found them to be consistently elevated in carriers of LRRK2 G2019S and R1441G/C as well as VPS35 D620N mutations. Urine BMP levels are promising biomarkers for patient stratification and potentially target engagement in clinical trials of emerging targeted PD therapies.

Retinal thickness may serve as a biomarker in Parkinson’s disease (PD). In this prospective longitudinal study, we aimed to determine if PD patients present accelerated thinning rate in the parafoveal ganglion cell-inner plexiform layer (pfGCIPL) and peripapillary retinal nerve fiber layer (pRNFL) compared to controls. Additionally, we evaluated the relationship between retinal neurodegeneration and clinical progression in PD. A cohort of 156 PD patients and 72 controls underwent retinal optical coherence tomography, visual, and cognitive assessments between February 2015 and December 2021 in two Spanish tertiary hospitals. The pfGCIPL thinning rate was twice as high in PD ( β [SE] = −0.58 [0.06]) than in controls ( β [SE] = −0.29 [0.06], p < 0.001). In PD, the progression pattern of pfGCIPL atrophy depended on baseline thickness, with slower thinning rates observed in PD patients with pfGCIPL below 89.8 µm. This result was validated with an external dataset from Moorfields Eye Hospital NHS Foundation Trust (AlzEye study). Slow pfGCIPL progressors, characterized by older at baseline, longer disease duration, and worse cognitive and disease stage scores, showed a threefold increase in the rate of cognitive decline ( β [SE] = −0.45 [0.19] points/year, p  = 0.021) compared to faster progressors. Furthermore, temporal sector pRNFL thinning was accelerated in PD ( β time x group [SE] = −0.67 [0.26] μm/year, p  = 0.009), demonstrating a close association with cognitive score changes ( β [SE] = 0.11 [0.05], p  = 0.052). This study suggests that a slower pattern of pfGCIPL tissue loss in PD is linked to more rapid cognitive decline, whereas changes in temporal pRNFL could track cognitive deterioration.

The Lebedev process, in which ethanol is catalytically converted into 1,3-butadiene, is an alternative process for the production of this commodity chemical. Silica–magnesia (SiO2–MgO) is a benchmark catalyst for the Lebedev process. Among the different preparation methods, the SiO2–MgO catalysts prepared by wet-kneading typically perform best owing to the surface magnesium silicates formed during wet-kneading. Although the thermal treatment is of pivotal importance as a last step in the catalyst preparation, the effect of the calcination temperature of the wet-kneaded SiO2–MgO on the Lebedev process has not been clarified yet. Here, we prepared and characterized in detail a series of wet-kneaded SiO2–MgO catalysts using varying calcination temperatures. We find that the thermal treatment largely influences the type of magnesium silicates, which have different catalytic properties. Our results suggest that the structurally ill-defined amorphous magnesium silicates and lizardite are responsible for the production of ethylene. Further, we argue that forsterite, which has been conventionally considered detrimental for the formation of ethylene, favors the formation of butadiene, especially when combined with stevensite.

Heterozygous gain-of-kinase function variants in LRRK2 (leucine-rich repeat kinase 2) cause 1–2% of all cases of Parkinson’s disease (PD) albeit with incomplete and age-dependent penetrance. All pathogenic LRRK2 mutations reside within the two catalytic domains of LRRK2—either in its kinase domain (e.g. G2019S) with modest effect or its ROC-COR GTPase domain (e.g. R1441G/H) with large effect on LRRK2 kinase activity. We have previously reported assays to interrogate LRRK2 kinase pathway activity in human bio-samples measuring phosphorylation of its endogenous substrate Rab10, that mirrors LRRK2 kinase activation status. Here, we isolated neutrophils from fresh peripheral blood from 101 participants including 42 LRRK2 mutation carriers (21 with the G2019S and 21 with the R1441G mutations), 27 patients with idiopathic PD, and 32 controls. Using a dual approach, LRRK2 dependent Rab10 phosphorylation at Threonine 73 (pRab10Thr73) was measured by quantitative multiplexed immunoblotting for pRab10Thr73/total Rab10 as well as targeted mass-spectrometry for absolute pRab10Thr73 occupancy. We found a significant over fourfold increase in pRab10Thr73 phosphorylation in carriers of the LRRK2 R1441G mutation irrespective of clinical disease status. The effect of the LRRK2 G2019S mutation did not reach statistical significance. Furthermore, we show that LRRK2 phosphorylation at Serine 935 is not a marker for LRRK2 kinase activity in human neutrophils. When analysing pRab10Thr73 phosphorylation in post-mortem brain samples, we observed overall high variability irrespective of clinical and LRRK2 mutation status and attributed this mainly to the adverse effect of the peri- and post-mortem period on the stability of posttranslational modifications such as protein phosphorylation. Overall, in vivo LRRK2 dependent pRab10Thr73 phosphorylation in human peripheral blood neutrophils is a specific, robust and promising biomarker for significant LRRK2 kinase hyperactivation, as with the LRRK2 R1441G mutation. Additional readouts and/or assays may be needed to increase sensitivity to detect modest LRRK2 kinase activation, as with the LRRK2 G2019S mutation. Our assays could be useful for patient stratification and target engagement studies for LRRK2 kinase inhibitors.

This review provides comprehensive aspects of the interaction of water with zeolites, focusing on its influence on the structural and catalytic properties of zeolites. It details how water can alter zeolite acidity by forming hydrogen bonding or hydronium ions through different modes of water in zeolite topologies. Moreover, it summarizes the risks of zeolite stability loss via hydrolysis of Si−O−T bonds to influence the stability, structure, and catalytic reactivity of zeolites. To address water interference, various strategies for water removal from zeolite frameworks are reviewed and proposed from the structural perspective of the zeolites. By combining advanced in‐situ techniques, FTIR and solid‐state NMR have proven effective in providing atomic‐level insights, as they eliminate the masking effects of water to enable precise characterization of the zeolite framework. This work underscores the importance of these methods in minimizing the influence of water, enhancing the reliability of zeolite characterization for catalytic applications, and providing insights into recent advancements, challenges, and future directions in the related fields. This review explores how water impacts zeolite structure, stability, and catalysis, including acidity modulation via hydrogen bonding and hydronium ion formation. It examines strategies for water removal from zeolites and highlights advanced in‐situ techniques, such as Fourier Transform Infrared (FTIR) spectroscopy and solid‐state Nuclear Magnetic Resonance (NMR), to achieve precise characterization. Insights into challenges and future advancements are provided.

Fluid catalytic cracking (FCC) is the major conversion process used in oil refineries to produce valuable hydrocarbons from crude oil fractions. Because the demand for oil-based products is ever increasing, research has been ongoing to improve the performance of FCC catalyst particles, which are complex mixtures of zeolite and binder materials. Unfortunately, there is limited insight into the distribution and activity of individual zeolitic domains at different life stages. Here we introduce a staining method to visualize the structure of zeolite particulates and other FCC components. Brønsted acidity maps have been constructed at the single particle level from fluorescence microscopy images. By applying a statistical methodology to a series of catalysts deactivated via industrial protocols, a correlation is established between Brønsted acidity and cracking activity. The generally applicable method has clear potential for catalyst diagnostics, as it determines intra- and interparticle Brønsted acidity distributions for industrial FCC materials. Insight into the active zeolitic domains of catalyst particles used in fluid catalytic cracking is limited by the particles' complex nature, but is crucial to improving these billion dollar catalysts. Now, a staining method allows confocal fluorescence microscopy to probe within single catalyst particles, and correlate Brønsted acidity distributions to catalytic activity.

Parkinson´s disease (PD) is a common neurodegenerative movement disorder and leucine-rich repeat kinase 2 (LRRK2) is a promising therapeutic target for disease intervention. However, the ability to stratify patients who will benefit from such treatment modalities based on shared etiology is critical for the success of disease-modifying therapies. Ciliary and centrosomal alterations are commonly associated with pathogenic LRRK2 kinase activity and can be detected in many cell types. We previously found centrosomal deficits in immortalized lymphocytes from G2019S-LRRK2 PD patients. Here, to investigate whether such deficits may serve as a potential blood biomarker for PD which is susceptible to LRKK2 inhibitor treatment, we characterized patient-derived cells from distinct PD cohorts. We report centrosomal alterations in peripheral cells from a subset of early-stage idiopathic PD patients which is mitigated by LRRK2 kinase inhibition, supporting a role for aberrant LRRK2 activity in idiopathic PD. Centrosomal defects are detected in R1441G-LRRK2 and G2019S-LRRK2 PD patients and in non-manifesting LRRK2 mutation carriers, indicating that they accumulate prior to a clinical PD diagnosis. They are present in immortalized cells as well as in primary lymphocytes from peripheral blood. These findings indicate that analysis of centrosomal defects as a blood-based patient stratification biomarker may help nominate idiopathic PD patients who will benefit from LRRK2-related therapeutics.