Modeling ammonia emissions from dairy production systems in the United States

Dairy production systems are hot spots of ammonia (NH3) emission. However, there remains large uncertainty in quantifying and mitigating NH3 emissions from dairy farms due to the lack of both long-term field measurements and reliable methods for extrapolating these measurements. In this study, a process-based biogeochemical model, Manure-DNDC, was tested against measurements of NH3 fluxes from five barns and one lagoon in four dairy farms over a range of environmental conditions and management practices in the United States. Results from the validation tests indicate that the magnitudes and seasonal patterns of NH3 fluxes simulated by Manure-DNDC were in agreement with the observations across the sites. The model was then applied to assess impacts of alternative management practices on NH3 emissions at the farm scale. The alternatives included reduction of crude protein content in feed, replacement of scraping with flushing for removal of manure from barn, lagoon coverage, increase in frequency for removal of slurry from lagoon, and replacement of surface spreading with incorporation for manure land application. The simulations demonstrate that: (a) all the tested alternative management practices decreased the NH3 emissions although the efficiency of mitigation varied; (b) a change of management in an upstream facility affected the NH3 emissions from all downstream facilities; and (c) an optimized strategy by combining the alternative practices on feed, manure removal, manure storage, and land application could reduce the farm-scale NH3 emission by up to 50%. The results from this study may provide useful information for mitigating NH3 emissions from dairy production systems and emphasize the necessity of whole-farm perspectives on the assessment of potential technical options for NH3 mitigation. This study also demonstrates the potential of utilizing process-based models, such as Manure-DNDC, to quantify and mitigate NH3 emissions from dairy farms

Symbolic bisimulation for quantum processes

With the previous notions of bisimulation presented in literature, to check if two quantum processes are bisimilar, we have to instantiate the free quantum variables of them with arbitrary quantum states, and verify the bisimilarity of resultant configurations. This makes checking bisimilarity infeasible from an algorithmic point of view because quantum states constitute a continuum. In this paper, we introduce a symbolic operational semantics for quantum processes directly at the quantum operation level, which allows us to describe the bisimulation between quantum processes without resorting to quantum states. We show that the symbolic bisimulation defined here is equivalent to the open bisimulation for quantum processes in the previous work, when strong bisimulations are considered. An algorithm for checking symbolic ground bisimilarity is presented. We also give a modal logical characterisation for quantum bisimilarity based on an extension of Hennessy-Milner logic to quantum processes.Comment: 30 pages, 7 figures, comments are welcom

ROLE OF THE REACTIVE OXYGEN SPECIES PEROXYNITRITE IN TRAUMATIC BRAIN INJURY

Reactive oxygen species (ROS) is cytotoxic to the cell and is known to contribute to secondary cell death following primary traumatic brain injury (TBI). We described in our study that PN is the main mediator for both lipid peroxidation and protein nitration, and occurred almost immediately after injury. As a downstream factor to oxidative damage, the peak of Ca2+-dependent, calpainmediated cytoskeletal proteolysis preceded that of neurodegeneration, suggesting that calpain-mediated proteolysis is the common pathway leading to neuronal cell death. The time course study clearly elucidated the interrelationship of these cellular changes following TBI, provided window of opportunity for pharmacological intervention. Furthermore, we conducted a pharmacological study to solidify our hypothesis. First of all, we tested the potency of a membrane permeable, catalytic scavenger of PN-derived free radicals, tempol for its ability to antagonize PN-induced oxidative damage. Tempol successfully inhibited PNinduced protein nitration at dosages of 30, 100 and 300mg/kg. Moreover, early single dose of 300mg/kg was administered and isolated mitochondria were examined for respiratory function and oxidative damage level. Our data showed that tempol reduced mitochondrial oxidative damage, and maintained mitochondrial function within normal limits, which suggested that tempol is efficiently permeable to mitochondrial membrane and mitochondrial oxidative damage is essential to mitochondrial dysfunction. Next, we found that calpainmediated proteolysis is reduced at early treatment with a single dose of tempol. However, the effect of tempol on calpain is short-lived possibly due to systematic elimination. In our multiple dose study, tempol showed a significant inhibitory effect on SBDPs. Consequently, we measured neuordegeneration with the de Olmos aminocupric silver staining method at 7 days post-injury and detected a significant decrease of neuronal cell death. Together, the time course study and pharmacological study strongly support the hypothesis that PN is the upstream mediator in secondary cell death in the CCI TBI mouse model. Moreover, inhibition of PN-mediated oxidative damage with the antioxidant, tempol, is able to attenuate multiple downstream injury mechanisms. However, targeting PN alone may be clinically impractical due to its limited therapeutic window. This limitation may be overcome in future studies by a combination of multiple therapeutic strategies