Are there Carbon Savings from US Biofuel Policies? Accounting for Leakage in Land and Fuel Markets

This paper applies the insights of the carbon leakage literature to study the emissions consequences of biofuel policies. We develop a simple analytic framework to decompose the intended emissions impacts of biofuel policy from four sources of carbon leakage: domestic fuel markets, domestic land markets, world land markets and world crude oil markets. A numerical simulation model illustrates the magnitude of each source of leakage for combinations of two current US biofuel policies: the Volumetric Ethanol Excise Tax Credit (VEETC) and the Renewable Fuel Standard (RFS). In the presence of both land and fuel market leakage, current US biofuel policies are unlikely to reduce greenhouse gases. Four of the five policy scenarios we consider lead to increases in greenhouse gas emissions. That is, total leakage was greater than 100%. The single scenario that generates emissions savings, the removal of the VEETC in conjunction with a binding RFS, only does so because negative leakage in the domestic fuel market offset the remaining positive sources of leakage.Multi-market, carbon leakage, biofuels, greenhouse gases, Agricultural and Food Policy, Land Economics/Use, Resource /Energy Economics and Policy, Q42, Q54, Q58,

A unique biofilm in human deep mycoses: fungal amyloid is bound by host serum amyloid P component

Background/Objectives We have demonstrated the presence of Candida cell surface amyloids that are important in aggregation of fungi and adherence to tissue. Fungal amyloid was present in invasive human candidal infections and host serum amyloid P component (SAP) bound to the fungal amyloid. SAP is a protease-resistant glycoprotein that binds avidly to amyloid and interferes with host defence, especially against bacterial pathogens for which neutrophils are important. In this study, we investigated whether biofilm of fungal amyloid and SAP was a feature of other disseminated fungal infections. Methods Tissue specimens from 15 autopsies were systematically evaluated with multiple histochemical stains including thioflavin T and Congo red (dyes that stain amyloid), as well as antibody to SAP. We studied specimens with disseminated aspergillosis, mucormycosis and coccidioidomycosis. The structure of the lesions, host inflammatory cells and the presence of fungal amyloid and SAP were determined. Results The structure of the lesions was characteristic in aspergillosis (‘starburst’) and mucormycosis (closely apposed bundles of hyphae). Host inflammatory cells were absent or few in number within these lesions. In Coccidioides lesions, host inflammation was sparse as well. Fungal amyloid was a prominent feature of all lesions along with abundant SAP bound to hyphae and spherules. Fungal amyloid and SAP perhaps contributed to persistence in caseous necrosis lesions. SAP also bound to Aspergillus and Mucorales amyloid in vitro. Conclusions A biofilm including amyloid and SAP is present in invasive fungal infections. This biofilm may dampen host defence leading to the characteristic sparse inflammatory reaction found in these infections

A Helminth Protease Inhibitor Modulates the Lipopolysaccharide-Induced Proinflammatory Phenotype of Microglia in vitro

Objective: The aim of this study was to examine whether the natural protease inhibitor Av-cystatin (rAv17) of the parasitic nematode Acanthocheilonema viteae exerts anti-inflammatory effects in an in vitro model of lipopolysaccharide (LPS)-activated microglia. Methods: Primary microglia were harvested from the brains of 2-day-old Wistar rats and cultured with or without rAv17 (250 nM). After 6 and 24 h the release of nitric oxide (Griess reagent) and TNF-α (ELISA) was measured in the supernatant. Real-time PCR was performed after 2, 6 and 24 h of culture to measure the mRNA expression of IL-1β, IL-6, TNF-α, COX-2, iNOS and IL-10. To address the involved signaling pathways, nuclear NF-ĸB translocation was visualized by immunocytochemistry. Morphological changes of microglia were analyzed by Coomassie blue staining. Differences between groups were calculated using one-way ANOVA with Bonferroni's post hoc test. Results: Morphological analysis indicated that LPS-induced microglial transformation towards an amoeboid morphology is inhibited by rAv17. Av-cystatin caused a time-dependent downregulation of proinflammatory cytokines, iNOS and COX-2 mRNA expression, respectively. This was paralleled by an upregulated expression of IL-10 in resting as well as in LPS-stimulated microglia. Av-cystatin reduced the release of NO and TNF-α in the culture supernatant. Immunocytochemical staining demonstrated an attenuated translocation of NF-ĸB by Av-cystatin in response to LPS. In addition, Western blot analysis revealed a rAv17-dependent reduction of the LPS-induced ERK1/2-pathway activation. Conclusion: The parasite-derived secretion product Av-cystatin inhibits proinflammatory mechanisms of LPS-induced microglia with IL-10, a potential key mediator.Peer Reviewe

Estimation of field production profiles in case of asphaltene deposition

In this work, we aimed to predict possible field production scenarios in case of asphaltene deposition based on field data as well as recommend remediation and stimulation measures to mitigate the risks of asphaltene deposition in the reservoir. We considered the influence of asphaltene formation in the near-wellbore of producers on the production data without reservoir pressure maintenance system in one of the oil fields. The asphaltene envelope in the reservoir oil was obtained, and the operating conditions of the field were evaluated under the possibility of asphaltene deposition. According to the results of dynamic modeling, the pressure map was plotted and the low-pressure areas in the near-wellbore were shown, which contributes to the aggravation of the problem associated with the asphaltene envelope. Based on the geometrical features of the low-pressure area, the dependence of the permeability reduction in the near-wellbore of the production well on the operating time was obtained using the asphaltene deposition model proposed by Wang and Civan. Based on the Buckley-Leverett theory, the field production profiles were calculated with and without asphaltene deposition. A decrease in the oil rate and consequently, the decrease in cumulative oil production in the field is expected due to the damage formation by solids. Maintenance of the production level will be facilitated by treating the nearwellbore with aromatic solvents and maintaining the reservoir pressure above the asphaltene onset pressure

Particle-particle particle-mesh method for dipolar interactions:on error estimates and efficiency of schemes with analytical differentiation and mesh interlacing

The interlaced and non-interlaced versions of the dipolar particle-particle particle-mesh (P3M) method implemented using the analytic differentiation scheme (AD-P3M) are presented together with their respective error estimates for the calculation of the forces, torques, and energies. Expressions for the optimized lattice Green functions, and for the Madelung self-forces, self-torques and self-energies are given. The applicability of the theoretical error estimates are thoroughly tested and confirmed in several numerical examples. Our results show that the accuracy of the calculations can be improved substantially when the approximate (mesh computed) Madelung self-interactions are subtracted. Furthermore, we show that the interlaced dipolar AD-P3M method delivers a significantly higher accuracy (which corresponds approximately to using a twice finer mesh) than the conventional method, allowing thereby to reduce the mesh size with respect to the non-interlaced version for a given accuracy. In addition, we present similar expressions for the dipolar ik-differentiation interlaced scheme, and we perform a comparison with the AD interlaced scheme. Rough tests for the relative speed of the dipolar P3M method using ik-differentiation and the interlaced/non-interlaced AD schemes show that when FFT computing time is the bottleneck, usually when working at high precisions, the interlaced AD-scheme can be several times faster than the other two schemes. For calculations with a low accuracy requirement, the interlaced version can perform worse than the ik and the non-interlaced AD schemes.All authors are grateful to the DAAD organization for providing financial support. C.H. thanks the DFG for support through the SimTech center of excellence, the ScaFaCoS collaboration, and the SFB 716, and acknowledges helpful discussions with A. Arnold and M. Pippig.Peer reviewe

Requirement of Estrogen Receptor-α in Insulin-like Growth Factor-1 (IGF-1)-induced Uterine Responses and in Vivo Evidence for IGF-1/Estrogen Receptor Cross-talk

In the uterus insulin-like growth factor-1 (IGF-1) signaling can be initiated by estradiol acting through its nuclear receptor (estrogen receptor (ER)) to stimulate the local synthesis of IGF-1. Conversely, in vitro studies have demonstrated that estradiol-independent ER transcriptional activity can be induced by IGF-1 signaling, providing evidence for a cross-talk mechanism between IGF-1 and ER. To investigate whether ER alpha is required for uterine responses to IGF-1 in vivo, both wild-type (WT) and ER alpha knockout (alpha ERKO) mice were administered IGF-1, and various uterine responses to IGF-1 were compared. In both WT and alpha ERKO mice, IGF-1 treatment resulted in phosphorylation of uterine IGF-1 receptor (IGF-1R) and formation of an IGF-1R/insulin receptor substrate-1/ phosphatidylinositol 3-kinase signaling complex. In addition, IGF-1 stimulated phosphorylation of uterine Akt and MAPK in both WT and alpha ERKO mice. However, IGF-1 treatment stimulated BrdUrd incorporation and proliferating cell nuclear antigen expression in WT uteri only. To determine whether ER alpha can be activated in vivo by IGF-1 signaling, transgenic mice carrying a luciferase gene driven by two estrogen response elements (ERE-luciferase mice) were utilized. Treatment of ovariectomized ERE-luciferase mice with IGF-1 resulted in an increase in uterine luciferase activity that was attenuated in the presence of the ER antagonist ICI 182,780. Together these data demonstrate that 1) functional signaling proximal to IGF-1R is maintained in the alpha ERKO mouse uterus, 2) ER alpha is necessary for IGF-1 induction of uterine nuclear proliferative responses, and 3) cross-talk between IGF-1R and ER signaling pathways exists in vivo

Serum Amyloid P Component Binds Fungal Surface Amyloid and Decreases Human Macrophage Phagocytosis and Secretion of Inflammatory Cytokines

In patients with invasive fungal diseases, there is often little cellular inflammatory response. We tested the idea that binding of the human constitutive plasma protein serum amyloid P component (SAP) (also called PTX2) to Candida albicans dampens the innate immune response to this fungus. Many pathogenic fungi have cell surface amyloid-like structures important for adhesion and biofilm formation. Human SAP bound to fungi that expressed functional cell surface amyloid, but SAP had minimal binding to fungi with reduced expression of cell surface amyloid. In the absence of SAP, phagocytosis of fungi by human macrophages was potentiated by expression of amyloid on the fungi. SAP binding to fungi inhibited their phagocytosis by macrophages. Macrophages pretreated with SAP displayed reduced fungal phagocytosis, reduced secretion of inflammatory cytokines (IFN, IL-6, and TNF), and increased secretion of the anti-inflammatory cytokine IL-10. SAP bound to fungi or added to the medium upregulated the expression of the antiinflammatory receptor CD206 on macrophages. These findings suggest that SAP bound to amyloid-like structures on fungal cells dampens the host cellular immune response in fungal diseases such as invasive candidiasis