Oxidative Desulphurization of Diesel Fuels

Oxidative desulphurization (ODS) enables attainment of ultra-low sulphur content in diesel fuels by oxidation of refractory sulphur compounds that are difficult to remove with hydrodesulphurization when the sulphur content needs to be attained below 10 mg kg–1. In this work, the effect of the process conditions of ultrasound-assisted ODS (using N,N-dimethylformamide and methanol as extraction solvents) on real diesel fuels was researched. The experiments were conducted in a batch reactor with hydrogen peroxide as oxidant and acetic acid as catalyst. Temperature increase, reaction time extension, and increase in the amount of dibenzothiophene (DBT) in real diesel fuels showed a positive impact on the ODS process efficiency. Comparison of ultrasound-assisted ODS and ODS in a mechanically stirred system revealed a significant reduction in reaction time. The very low sulphur concentrations (3 mg kg–1) in the product obtained after 30 minutes of oxidation confirmed high efficiency of the oxidative desulphurization

Laboratory coupling approach

This chapter deals with the coupling of smart grid laboratories for joint experiments. Therefore, various possibilities are outlined and a reference implementation is introduced. Finally, the vision of a distributed, virtual research infrastructure is presented

The Targeting of Plasmalemmal Ceramide to Mitochondria during Apoptosis

Ceramide is a key lipid mediator of cellular processes such as differentiation, proliferation, growth arrest and apoptosis. During apoptosis, ceramide is produced within the plasma membrane. Although recent data suggest that the generation of intracellular ceramide increases mitochondrial permeability, the source of mitochondrial ceramide remains unknown. Here, we determine whether a stress-mediated plasmalemmal pool of ceramide might become available to the mitochondria of apoptotic cells. We have previously established annexin A1—a member of a family of Ca2+ and membrane-binding proteins—to be a marker of ceramide platforms. Using fluorescently tagged annexin A1, we show that, upon its generation within the plasma membrane, ceramide self-associates into platforms that subsequently invaginate and fuse with mitochondria. An accumulation of ceramide within the mitochondria of apoptotic cells was also confirmed using a ceramide-specific antibody. Electron microscopic tomography confirmed that upon the formation of ceramide platforms, the invaginated regions of the plasma membrane extend deep into the cytoplasm forming direct physical contacts with mitochondrial outer membranes. Ceramide might thus be directly transferred from the plasma membrane to the mitochondrial outer membrane. It is conceivable that this “kiss-of-death” increases the permeability of the mitochondrial outer membrane thereby triggering apoptosis

Transient Alteration of Cellular Redox Buffering before Irradiation Triggers Apoptosis in Head and Neck Carcinoma Stem and Non-Stem Cells

Background: Head and neck squamous cell carcinoma (HNSCC) is an aggressive and recurrent malignancy owing to intrinsic radioresistance and lack of induction of apoptosis. The major focus of this work was to design a transient glutathione depleting strategy during the course of irradiation of HNSCC in order to overcome their radioresistance associated with redox adaptation. Methodology/Principal Findings: Treatment of SQ20B cells with dimethylfumarate (DMF), a GSH-depleting agent, and L-Buthionine sulfoximine (BSO), an inhibitor of GSH biosynthesis 4 h before a 10 Gy irradiation led to the lowering of the endogenous GSH content to less than 10 % of that in control cells and to the triggering of radiation-induced apoptotic cell death. The sequence of biochemical events after GSH depletion and irradiation included ASK-1 followed by JNK activation which resulted in the triggering of the intrinsic apoptotic pathway through Bax translocation to mitochondria. Conclusions: This transient GSH depletion also triggered radiation-induced cell death in SQ20B stem cells, a key event to overcome locoregional recurrence of HNSCC. Finally, our in vivo data highlight the relevance for further clinical trials o

The role of the mitochondria and the endoplasmic reticulum contact sites in the development of the immune responses

Abstract Mitochondria and endoplasmic reticulum (ER) contact sites (MERCs) are dynamic modules enriched in subset of lipids and specialized proteins that determine their structure and functions. The MERCs regulate lipid transfer, autophagosome formation, mitochondrial fission, Ca2+ homeostasis and apoptosis. Since these functions are essential for cell biology, it is therefore not surprising that MERCs also play a critical role in organ physiology among which the immune system stands by its critical host defense function. This defense system must discriminate and tolerate host cells and beneficial commensal microorganisms while eliminating pathogenic ones in order to preserve normal homeostasis. To meet this goal, the immune system has two lines of defense. First, the fast acting but unspecific innate immune system relies on anatomical physical barriers and subsets of hematopoietically derived cells expressing germline-encoded receptors called pattern recognition receptors (PRR) recognizing conserved motifs on the pathogens. Second, the slower but very specific adaptive immune response is added to complement innate immunity. Adaptive immunity relies on another set of specialized cells, the lymphocytes, harboring receptors requiring somatic recombination to be expressed. Both innate and adaptive immune cells must be activated to phagocytose and process pathogens, migrate, proliferate, release soluble factors and destroy infected cells. Some of these functions are strongly dependent on lipid transfer, autophagosome formation, mitochondrial fission, and Ca2+ flux; this indicates that MERCs could regulate immunity

Increased hormonal stress reactions induced in an Alpine Black Grouse (Tetrao tetrix) population by winter sports

In the Italian Alps the intensification of winter sports represents an increasing threat for Black Grouse (Tetrao tetrix). During the winters 2010/2011 and 2011/2012, characterised by different amounts of snowfall, 58 droppings from as many snow burrows were collected in three areas with different human disturbance to evaluate its effects on Black Grouse stress responses. Subjects in highly disturbed area showed higher concentrations of corticosterone metabolites during the winter with high snow cover highlighting a relationship between animals' stress and regular winter sports. As human-induced stress may contribute to population decline, tourism management should be planned to support Grouse conservation

Evaluation of the physiological stress response induced by winter sports in a black grouse (Tetrao tetrix) population from Lepontine Alps

In the Alps, human outdoor leisure activities are an increasing conservation issue having a strong impact on wildlife, mainly on endangered species, such as black grouse (Tetrao tetrix). Since freeriding sports are one factor affecting this species, it is important to quantify the likely pressure of recreational disturbance on their health status considering that induced stress can alter animal fitness. Using a non-invasive technique we examined the physiological stress response of a black grouse population from Central Alps induced by snow sports in relation to areas with different humandisturbance. During two winters (2011 and 2012) we sampled 58 fresh droppings from as many snow burrows to analyse concentrations of corticosterone metabolites (CM) by an enzyme immunoassay (EIA). In 2011, faecal CM levels in high human-disturbance areas were significantly higher (mean: 512\ub1107 ng/g) than those in moderate (151\ub142 ng/g) and low disturbed (138\ub142 ng/g) ones, moreover higher CM concentrations were observed in areas closer to ski lifts. On the contrary, in 2012, no signifi cant differences in CM values were found between areas. Comparing results from sampling areas between study years, high-disturbed area CM levels were significantly higher in 2011 (m2011: 512 ng/g; m2012: 178 ng/g) while no significant differences were observed in moderate (m2011: 151 ng/g; m2012: 178 ng/g) and low (m2011: 138 ng/g; m2012: 211 ng/g) human-disturbed areas. Data show a great difference in high-disturbed areas CM levels between sampling years: in winter 2011 regular snowfalls have favoured the presence of skiers that elevate stress values and could represent a further threat to the fi tness of black grouse. In 2012 the lack of snow has drastically reduced winter sports with a consequent lower human disturbance, reflected to CM levels. Moreover in 2012 the increase of population baseline CM values in low disturbed areas suggest a more stressful condition as they have to acclimate to these unusual meteorological trends

Identification of Novel Cyclic Lipopeptides from a Positional Scanning Combinatorial Library with Enhanced Antibacterial and Antibiofilm Activities

Treating bacterial infections can be difficult due to innate or acquired resistance mechanisms, and the formation of biofilms. Cyclic lipopeptides derived from fusaricidin/LI-F natural products represent particularly attractive candidates for the development of new antibacterial and antibiofilm agents, with the potential to meet the challenge of bacterial resistance to antibiotics. A positional-scanning combinatorial approach was used to identify the amino acid residues responsible for driving antibacterial activity, and increase the potency of these cyclic lipopeptides. Screening against the antibiotic resistant ESKAPE pathogens revealed the importance of hydrophobic as well as positively charged amino acid residues for activity of this class of peptides. The improvement in potency was especially evident against bacterial biofilms, since the lead cyclic lipopeptide showed promising in vitro and in vivo anti-biofilm activity at the concentration far below its respective MICs. Importantly, structural changes resulting in a more hydrophobic and positively charged analog did not lead to an increase in toxicity toward human cells