The mechanism of the selective reduction of nitrogen oxides by hydrocarbons on zeolite catalysts

The mechanism of the selective catalytic reduction (SCR) of nitrogen oxides over 3d transition metal zeolites has been investigated in a variety of ways. The initial step is the abstraction of hydrogen from the hydrocarbon by adsorbed NO₂ species which is rate determining with methane but not with isobutane. The subsequent path appears to involve nitroso and/or nitro compounds. Comparative studies of the reactions of such compounds indicate that nitromethane is more likely to be an intermediate than nitrosomethane during the methane-SCR reaction over Co-MFI although the latter cannot be ruled out entirely. In both cases the predominant route to N₂ is an initial decomposition to carbon oxides and ammonia followed by the NH₃-SCR reaction. The isobutane-SCR reaction over Fe-MFI produces substantial amounts of hydrogen cyanide which disappears only at temperatures where all the hydrocarbon has been consumed. Hydrogen cyanide appears to arise from isobutyronitrile, the expected dehydration product if an initially formed nitroso compound undergoes tautomerism to an oxime. HCN is converted to N₂ largely by reaction with NO₂ which is fast well below 300°C in the absence of isobutane. The corresponding isobutane-SCR reaction over Cu-MFI gives rise to cyanogen (C₂N₂) rather than HCN. The general path is probably the same in the two systems with the difference arising from variation in the relative reactivity of HCN. The copper-containing catalyst is very effective at forming and dimerising adsorbed cyanide groups while the iron catalyst has higher activity for the oxidation of NO to the NO₂ needed to convert adsorbed cyanide to N₂. The difference between the apparent involvement of a nitro route in methane-SCR with Co-MFI, and a nitroso one with isobutane, is similarly explainable. The former reaction proceeds with simultaneous production of NO₂ which can participate in the intermediate chemistry that follows. However, the NO₂ concentration is low during the latter reaction over Cu-MFI and Fe-MFI as long as any hydrocarbon remains. This is due to the blocking of sites for NO oxidation by deposits and the recycling of NO₂ back to NO during hydrocarbon oxidation. Thus only NO is available and the nitroso route prevails. The extent to which this picture applies with other catalysts and other hydrocarbons remains to be established.     

Flux and traction boundary elements without hypersingular or strongly singular integrals

The present paper deals with a boundary element formulation based on the traction elasticity boundary integral equation (potential derivative for Laplace's problem). The hypersingular and strongly singular integrals appearing in the formulation are analytically transformed to yield line and surface integrals which are at most weakly singular. Regularization and analytical transformation of the boundary integrals is done prior to any boundary discretization. The integration process does not require any change of co‐ordinates and the resulting integrals can be numerically evaluated in a simple and efficient way. The formulation presented is completely general and valid for arbitrary shaped open or closed boundaries. Analytical expressions for all the required hypersingular or strongly singular integrals are given in the paper. To fulfil the continuity requirement over the primary density a simple BE discretization strategy is adopted. Continuous elements are used whereas the collocation points are shifted towards the interior of the elements. This paper pretends to contribute to the transformation of hypersingular boundary element formulations as something clear, general and easy to handle similar to in the classical formulation. Copyright © 2000 John Wiley & Sons, Ltd.     

A Comprehensive Biomarker Analysis of Microsatellite Unstable/Mismatch Repair Deficient Colorectal Cancer Cohort Treated with Immunotherapy

The search for immunotherapy biomarkers in Microsatellite Instability High/Deficient Mismatch Repair system (MSI-H/dMMR) metastatic colorectal cancer (mCRC) is an unmet need. Sixteen patients with mCRC and MSI-H/dMMR (determined by either immunohistochemistry or polymerase chain reaction) treated with PD-1/PD-L1 inhibitors at our institution were included. According to whether the progression-free survival with PD-1/PD-L1 inhibitors was longer than 6 months or shorter, patients were clustered into the IT-responder group (n: 9 patients) or IT-resistant group (n: 7 patients), respectively. In order to evaluate determinants of benefit with PD-1/PD-L1 inhibitors, we performed multimodal analysis including genomics (through NGS panel tumour-only with 431 genes) and the immune microenvironment (using CD3, CD8, FOXP3 and PD-L1 antibodies). The following mutations were more frequent in IT-resistant compared with IT-responder groups: B2M (4/7 versus 2/9), CTNNB1 (2/7 versus 0/9), and biallelic PTEN (3/7 versus 1/9). Biallelic ARID1A mutations were found exclusively in the IT-responder group (4/9 patients). Tumour mutational burden did not correlate with immunotherapy benefit, neither the rate of indels in homopolymeric regions. Of note, biallelic ARID1A mutated tumours had the highest immune infiltration and PD-L1 scores, contrary to tumours with CTNNB1 mutation. Immune microenvironment analysis showed higher densities of different T cell subpopulations and PD-L1 expression in IT-responders. Misdiagnosis of MSI-H/dMMR inferred by discordances between immunohistochemistry and polymerase chain reaction was only found in the IT-resistant population (3/7 patients). Biallelic ARID1A mutations and Wnt signalling activation through CTNNB1 mutation were associated with high and low T cell immune infiltrates, respectively, and deserve special attention as determinants of response to PD-1/PD-L1 inhibitors. The non-MSI-H phenotype in dMMR is associated with poor benefit to immunotherapy. Our results suggest that mechanisms of resistance to immunotherapy are multi-factorial.     

Nickel–carbon nanocomposites prepared using castor oil as precursor: A novel catalyst for ethanol steam reforming

A novel and simple method to prepare nickel-based catalysts for ethanol steam reforming is proposed. The present method was developed using castor oil as a precursor. The results clarify that the nickel–carbon (Ni/C) catalyst has a high activity for ethanol steam reforming. It was observed that the catalytic behavior could be modified according to the experimental conditions employed. Moreover, it is interesting to note that the increase in the catalytic activity of the Ni/C nanocomposite over time, at 500 and 600 °C of reaction temperature, may be associated with the formation of filamentous carbon. The preliminary results indicate that the novel methodology used, led to the obtainment of materials with important properties that can be extended to applications in different catalytic process.     

Differences in Tau Seeding in Newborn and Adult Wild-Type Mice

Alzheimer’s disease (AD) and other tauopathies are common neurodegenerative diseases in older adults; in contrast, abnormal tau deposition in neurons and glial cells occurs only exceptionally in children. Sarkosyl-insoluble fractions from sporadic AD (sAD) containing paired helical filaments (PHFs) were inoculated unilaterally into the thalamus in newborn and three-month-old wild-type C57BL/6 mice, which were killed at different intervals from 24 h to six months after inoculation. Tau-positive cells were scanty and practically disappeared at three months in mice inoculated at the age of a newborn. In contrast, large numbers of tau-positive cells, including neurons and oligodendrocytes, were found in the thalamus of mice inoculated at three months and killed at the ages of six months and nine months. Mice inoculated at the age of newborn and re-inoculated at the age of three months showed similar numbers and distribution of positive cells in the thalamus at six months and nine months. This study shows that (a) differences in tau seeding between newborn and young adults may be related to the ratios between 3Rtau and 4Rtau, and the shift to 4Rtau predominance in adults, together with the immaturity of connections in newborn mice, and (b) intracerebral inoculation of sAD PHFs in newborn mice does not protect from tau seeding following intracerebral inoculation of sAD PHFs in young/adult mice.     

NRN1 Gene as a Potential Marker of Early-Onset Schizophrenia: Evidence from Genetic and Neuroimaging Approaches

Included in the neurotrophins family, the Neuritin 1 gene (NRN1) has emerged as an attractive candidate gene for schizophrenia (SZ) since it has been associated with the risk for the disorder and general cognitive performance. In this work, we aimed to further investigate the association of NRN1 with SZ by exploring its role on age at onset and its brain activity correlates. First, we developed two genetic association analyses using a family-based sample (80 early-onset (EO) trios (offspring onset ≤ 18 years) and 71 adult-onset (AO) trios) and an independent case–control sample (120 healthy subjects (HS), 87 EO and 138 AO patients). Second, we explored the effect of NRN1 on brain activity during a working memory task (N-back task; 39 HS, 39 EO and 39 AO; matched by age, sex and estimated IQ). Different haplotypes encompassing the same three Single Nucleotide Polymorphisms(SNPs, rs3763180–rs10484320–rs4960155) were associated with EO in the two samples (GCT, TCC and GTT). Besides, the GTT haplotype was associated with worse N-back task performance in EO and was linked to an inefficient dorsolateral prefrontal cortex activity in subjects with EO compared to HS. Our results show convergent evidence on the NRN1 association with EO both from genetic and neuroimaging approaches, highlighting the role of neurotrophins in the pathophysiology of SZ.     

Effect of different concentrations of carbon dioxide and low concentration of carbon monoxide on the shelf-life of fresh pork sausages packaged in modified atmosphere

This paper reports the effects of different concentrations of carbon dioxide and the presence of low levels of carbon monoxide on quality attributes throughout storage of fresh pork sausages. Four pork forelegs (initial pH 5.5-5.7) were used to prepare a total of 120 fresh sausages, which were packaged in different atmospheres containing (%O(2)/%CO(2)/%N(2)): 0/20/80; 0/60/40; 40/20/40; 40/60/0; 80/20/0; and 0.3% CO/30% CO(2)/rest argon. The packs were stored for 20 days at 2±1 °C in the dark. Three packs for each atmosphere were opened every 4 days for subsequent analysis of pH, colour CIE L*, a*, b*, TBARS formation, microbial psychotrophic aerobes and sensory discolouration and off-odour. Results showed that increasing concentrations of carbon dioxide promoted oxidation of both myoglobin and lipids, most probably due to its effect of lowering pH. Therefore, preservation of colour and odour of fresh pork sausages packaged in modified atmosphere was better achieved using atmospheres containing low CO(2) concentrations (20%) rather than high (60%). However, their shelf-life depended also on the concentration of O(2); 20% CO(2) with high O(2) (80%) enhanced the red colour, but shortened shelf-life, while 20% CO(2) in the absence of O(2) extended freshness to 16 days. The atmosphere containing 0.3% CO, together with 30% CO(2), maintained the red colour for 20 days, but failed to keep fresh odour longer than 16 days.     

Effects of Hypocalcemic Vitamin D Analogs in the Expression of DNA Damage Induced in Minilungs from hESCs: Implications for Lung Fibrosis

In our previous work, we evaluated the therapeutic effects of 1α,25-Dihydroxyvitamin D₃, the biologically active form of vitamin D, in the context of bleomycin-induced lung fibrosis. Contrary to the expected, vitamin D supplementation increased the DNA damage expression and cellular senescence in alveolar epithelial type II cells and aggravated the overall lung pathology induced in mice by bleomycin. These effects were probably due to an alteration in the cellular DNA double-strand breaks’ repair capability. In the present work, we have evaluated the effects of two hypocalcemic vitamin D analogs (calcipotriol and paricalcitol) in the expression of DNA damage in the context of minilungs derived from human embryonic stem cells and in the cell line A549.     

Molecular Mechanisms of Kidney Injury and Repair

Chronic kidney disease (CKD) will become the fifth global cause of death by 2040, thus emphasizing the need to better understand the molecular mechanisms of damage and regeneration in the kidney. CKD predisposes to acute kidney injury (AKI) which, in turn, promotes CKD progression. This implies that CKD or the AKI-to-CKD transition are associated with dysfunctional kidney repair mechanisms. Current therapeutic options slow CKD progression but fail to treat or accelerate recovery from AKI and are unable to promote kidney regeneration. Unraveling the cellular and molecular mechanisms involved in kidney injury and repair, including the failure of this process, may provide novel biomarkers and therapeutic tools. We now review the contribution of different molecular and cellular events to the AKI-to-CKD transition, focusing on the role of macrophages in kidney injury, the different forms of regulated cell death and necroinflammation, cellular senescence and the senescence-associated secretory phenotype (SAPS), polyploidization, and podocyte injury and activation of parietal epithelial cells. Next, we discuss key contributors to repair of kidney injury and opportunities for their therapeutic manipulation, with a focus on resident renal progenitor cells, stem cells and their reparative secretome, certain macrophage subphenotypes within the M2 phenotype and senescent cell clearance.