Mechanism and kinetics of the reduction of nitric oxide by granular activated carbon induced by PdO/Ai2O3 in the presence of O2

NOx and particulate matter are the main environmental hazards found in Diesel exhaust. In order to explore a novel method to remove NOx as well as particulate matter, we examined the catalytic reduction of NOx with solid carbonaceous materials as a surrogate for soot in the presence of oxygen. Pd loaded on Al2O3 has been found to be an active catalyst that resists S and H2O poisoning. A catalyst containing of 2.5% PdO on Al203 exhibits as high as 90% conversion of NO to N2 at space velocities of up to 50,000 hr and at 500°C. Most of the experiments were conducted with a feed gas containing 590 ppm NO, 10% oxygen and the balance He as a function of space velocity in the range of 12,000 to 90,000 hr-1 and temperature in the range of 350 to 550°C. The result shows that a stable intermediate, CO, is formed by the oxidation of granular activated carbon (GAC) with 02, and the rate controlling step of the proposed reaction mechanism for the NO reduction is the reaction of NO + CO. Kinetic experiments were carried out in a fixed bed reactor to determine the apparent reaction order and activation energy of the rate determining step. It was found that the activation energy for the rate determine step was 24.1 kcal/mol. The apparent activation energy for the pore diffusion controlled region was 8.97 kcal/mol. Having an apparent activation energy below 10 kcal/mol. indicate that pore diffusion is the likely mechanism in this region

Dysregulated Interferon Response Underlying Severe COVID-19

Innate immune interferons (IFNs), including type I and III IFNs, constitute critical antiviral mechanisms. Recent studies reveal that IFN dysregulation is key to determine COVID-19 pathogenesis. Effective IFN stimulation or prophylactic administration of IFNs at the early stage prior to severe COVID-19 may elicit an autonomous antiviral state, restrict the virus infection, and prevent COVID-19 progression. Inborn genetic flaws and autoreactive antibodies that block IFN response have been significantly associated with about 14% of patients with life-threatening COVID-19 pneumonia. In most severe COVID-19 patients without genetic errors in IFN-relevant gene loci, IFN dysregulation is progressively worsened and associated with the situation of pro-inflammation and immunopathy, which is prone to autoimmunity. In addition, the high correlation of severe COVID-19 with seniority, males, and individuals with pre-existing comorbidities will be plausibly explained by the coincidence of IFN aberrance in these situations. Collectively, current studies call for a better understanding of the IFN response regarding the spatiotemporal determination and subtype-specificity against SARS-CoV-2 infections, which are warranted to devise IFN-related prophylactics and therapies

Epigenetic Evolution of ACE2 and IL-6 Genes: Non-Canonical Interferon-Stimulated Genes Correlate to COVID-19 Susceptibility in Vertebrates

The current novel coronavirus disease (COVID-19) has spread globally within a matter of months. The virus establishes a success in balancing its deadliness and contagiousness, and causes substantial differences in susceptibility and disease progression in people of different ages, genders and pre-existing comorbidities. These host factors are subjected to epigenetic regulation; therefore, relevant analyses on some key genes underlying COVID-19 pathogenesis were performed to longitudinally decipher their epigenetic correlation to COVID-19 susceptibility. The genes of host angiotensin-converting enzyme 2 (ACE2, as the major virus receptor) and interleukin (IL)-6 (a key immuno-pathological factor triggering cytokine storm) were shown to evince active epigenetic evolution via histone modification and cis/trans-factors interaction across different vertebrate species. Extensive analyses revealed that ACE2 ad IL-6 genes are among a subset of non-canonical interferon-stimulated genes (non-ISGs), which have been designated for their unconventional responses to interferons (IFNs) and inflammatory stimuli through an epigenetic cascade. Furthermore, significantly higher positive histone modification markers and position weight matrix (PWM) scores of key cis-elements corresponding to inflammatory and IFN signaling, were discovered in both ACE2 and IL6 gene promoters across representative COVID-19-susceptible species compared to unsusceptible ones. The findings characterize ACE2 and IL-6 genes as non-ISGs that respond differently to inflammatory and IFN signaling from the canonical ISGs. The epigenetic properties ACE2 and IL-6 genes may serve as biomarkers to longitudinally predict COVID-19 susceptibility in vertebrates and partially explain COVID-19 inequality in people of different subgroups

Charged BTZ-like black hole solutions and the diffusivity-butterfly velocity relation

We show that there exists a class of charged BTZ-like black hole solutions in Lifshitz spacetime with a hyperscaling violating factor. The charged BTZ is characterized by a charge-dependent logarithmic term in the metric function. As concrete examples, we give five such charged BTZ-like black hole solutions and the standard charged BTZ metric can be regarded as a special instance of them. In order to check the recent proposed universal relations between diffusivity and the butterfly velocity, we first compute the diffusion constants of the standard charged BTZ black holes and then extend our calculation to arbitrary dimension $d$, exponents $z$ and $\theta$. Remarkably, the case $d=\theta$ and $z=2$ is a very special in that the charge diffusion $D_c$ is a constant and the energy diffusion $D_e$ might be ill-defined, but $v^2_B\tau$ diverges. We also compute the diffusion constants for the case that the DC conductivity is finite but in the absence of momentum relaxation.Comment: 30 pages, 2 figure

Integrate structural analysis, isoform diversity, and interferon-inductive propensity of ACE2 to predict SARS-CoV2 susceptibility in vertebrates

The current new coronavirus disease (COVID-19) has caused globally over 0.4/6 million confirmed deaths/infected cases across more than 200 countries. As the etiological coronavirus (a.k.a. SARS-CoV2) may putatively have a bat origin, our understanding about its intermediate reservoir between bats and humans, especially its tropism in wild and domestic animals are mostly unknown. This constitutes major concerns in public health for the current pandemics and potential zoonosis. Previous reports using structural analysis of the viral spike protein (S) binding its cell receptor of angiotensin-converting enzyme 2 (ACE2), indicate a broad potential of SARS-CoV2 susceptibility in wild and particularly domestic animals. Through integration of key immunogenetic factors, including the existence of S-binding-void ACE2 isoforms and the disparity of ACE2 expression upon early innate immune response, we further refine the SARS-CoV2 susceptibility prediction to fit recent experimental validation. In addition to showing a broad susceptibility potential across mammalian species based on structural analysis, our results also reveal that domestic animals including dogs, pigs, cattle and goats may evolve ACE2-related immunogenetic diversity to restrict SARS-CoV2 infections. Thus, we propose that domestic animals may be unlikely to play a role as amplifying hosts unless the virus has further species-specific adaptation. Findings may relieve relevant public concerns regarding COVID-19-like risk in domestic animals, highlight virus-host coevolution, and evoke disease intervention through targeting ACE2 molecular diversity and interferon optimization