Kinetic modelling of steam gasification of various woody biomass chars: influence of inorganic elements

A study was performed on the influence of wood variability on char steam gasification kinetics. Isothermal experiments were carried out in a thermobalance in chemical regime on various wood chars produced under the same conditions. The samples exhibited large differences of average reaction rate. These differences were linked neither with the biomass species nor age and may be related to the biomass inorganic elements. A modelling approach was developed to give a quantitative insight to these observations. The grain model was used on one biomass of reference for temperatures between 750 and 900 °C and steam partial pressures between 0 and 0.27 bar. The model was applied to the other samples through the addition of an integral parameter specific to each sample. A satisfactory correlation was found between this parameter and the ratio potassium/silicium. This result highlighted the catalytic effect of potassium and inhibitor effect of silicium on the reaction.     

CO2 induced seawater acidification impacts sea urchin larval development I: elevated metabolic rates decrease scope for growth and induce developmental delay

Anthropogenic CO(2) emissions are acidifying the world's oceans. A growing body of evidence is showing that ocean acidification impacts growth and developmental rates of marine invertebrates. Here we test the impact of elevated seawater pCO(2) (129 Pa, 1271 μatm) on early development, larval metabolic and feeding rates in a marine model organism, the sea urchin Strongylocentrotus purpuratus. Growth and development was assessed by measuring total body length, body rod length, postoral rod length and posterolateral rod length. Comparing these parameters between treatments suggests that larvae suffer from a developmental delay (by ca. 8%) rather than from the previously postulated reductions in size at comparable developmental stages. Further, we found maximum increases in respiration rates of +100% under elevated pCO(2), while body length corrected feeding rates did not differ between larvae from both treatments. Calculating scope for growth illustrates that larvae raised under high pCO(2) spent an average of 39 to 45% of the available energy for somatic growth, while control larvae could allocate between 78 and 80% of the available energy into growth processes. Our results highlight the importance of defining a standard frame of reference when comparing a given parameter between treatments, as observed differences can be easily due to comparison of different larval ages with their specific set of biological characters.     

Diversity of gut Bifidobacterium species is not altered between allergic and non-allergic French infants

Some clinical studies have suggested a relationship between allergic diseases and gut microbiota. We aimed to study bifidobacterial colonization at species and strain levels in ten allergic French infants included at their first clinical consultation and 20 controls matching for age at sampling, mode of delivery, per partum antibiotics, type of feeding and antibiotics in the first weeks of life. The faecal microbiota was analyzed by culture methods and TTGE. Bifidobacterial species and strains were identified using multiplex PCR and Box-PCR fingerprinting. No differences were observed between groups in the number of colonized infants or in the levels of colonization by the main aerobic and anaerobic genera. All infants were colonized with high levels of Bifidobacterium except for one in each group. One to 5 Bifidobacterium species and 1 to 7 strains were observed per subject independently of allergic status and age at sampling. Our study showed the infants to be colonized by several species and strains, including several strains from the same species. This diversity in Bifidobacterium colonization was not related with the allergic status and showed that the link between Bifidobacterium colonization and allergic diseases is complex and cannot be restricted to the role attributed to Bifidobacterium species.     

Anti-cetuximab IgE ELISA for identification of patients at a high risk of cetuximab-induced anaphylaxis

Cetuximab, a chimeric mouse-human IgG1 monoclonal antibody against the epidermal growth factor receptor, has proven effective in the treatment of metastatic colorectal cancer and squamous cell carcinoma of the head and neck. However, a high incidence of immediate hypersensitivity reactions (HSR) to cetuximab after the first infusion has been observed. We have developed a test for identification of patients likely to show treatment-related HSR to cetuximab. An enzyme-linked immunosorbent assay (ELISA) for detecting anti-cetuximab IgEs was developed and tested on serum samples collected from cancer patients before start of cetuximab treatment, and from healthy blood donors. Similar levels of anti-cetuximab IgE were detected in pre-treatment patient sera (24/92, 26.1%) and sera from healthy blood donors (33/117, 28.2%). HSR were observed in 14 out of the 92 patients (15.2%), and 8 of these (57.1%) were grade 3–4. Anti-cetuximab IgEs were detected in 7/8 of the patients (87.5%) with severe HSRs as compared with 14/78 patients (17.9%) with no HSR (p = 0.0002). Predictive value of the anti-cetuximab IgE test for HSR events of grades 3–4 was calculated using Receiver Operating Characteristics analysis. With a cut-off value of 29 arbitrary units for the anti-cetuximab IgE, the ELISA test showed a sensitivity of 87.5%, specificity of 82.1%, positive predictive value of 33.3% and negative predictive value of 98.5%. Anti-cetuximab IgE ELISA detection could be a valuable tool to help the physician anticipate an anaphylaxis episode following cetuximab infusion and opt for a suitable alternative treatment.Key words: anti-cetuximab antibodies, ELISA, hypersensitivity, therapeutic monoclonal antibody, ROC     

Calcium Oscillations

Calcium signaling results from a complex interplay between activation and inactivation of intracellular and extracellular calcium permeable channels. This complexity is obvious from the pattern of calcium signals observed with modest, physiological concentrations of calcium-mobilizing agonists, which typically present as sequential regenerative discharges of stored calcium, a process referred to as calcium oscillations. In this review, we discuss recent advances in understanding the underlying mechanism of calcium oscillations through the power of mathematical modeling. We also summarize recent findings on the role of calcium entry through store-operated channels in sustaining calcium oscillations and in the mechanism by which calcium oscillations couple to downstream effectors.Calcium ions participate in a multiplicity of physiological and pathological functions. Among the most intensely studied, and the major focus of this article, is the role of Ca²⁺ as a cellular signal. Elevations in cytoplasmic Ca²⁺ mediate a plethora of cellular responses, ranging from extremely rapid events (muscle contraction, neurosecretion), to slower more subtle responses (cell division, differentiation, apoptosis). In contrast to most cellular signals, it is a relatively simple matter to observe changes in cytoplasmic Ca²⁺ in real time in living cells. As a result, the truly complex nature of Ca²⁺ signaling pathways has been revealed. The challenge is to understand what regulates these signals and what the biological significance of their complexity is.In the majority of laboratory experiments examining effects of various stimulants on Ca²⁺ signaling, supramaximal concentrations of activating agonists are employed resulting in rapid, robust, and often sustained increases in cytoplasmic Ca²⁺. It has long been appreciated that these signals result from a coordinated release of intracellular stores and increased Ca²⁺ influx across the plasma membrane (Bohr, 1973; Putney et al. 1981). The intracellular release of Ca²⁺ most commonly results from the Ca²⁺ releasing action of the phospholipase C-derived second messenger, inositol 1,4,5-trisphosphate (InsP₃) (Streb et al. 1983), whereas the entry of Ca²⁺ is because of the activation of store-operated channels in the plasma membrane (Putney 1986). However, it is becoming increasingly clear that these large sustained elevations seldom occur with physiological levels of stimulants. Rather the more common pattern of Ca²⁺ signaling, in both excitable and nonexcitable cells is a pattern of periodic discharges and/or entry of Ca²⁺. In excitable cells, such as the heart for example, these may be comprised of, or initiated by regenerative all-or-none plasma membrane channel activation, the Ca²⁺ action potential (Tsien et al. 1986) with amplification by intracellular Ca²⁺ release (Fabiato 1983). In nonexcitable cells, these spikes of cytoplasmic Ca²⁺ arise from regenerative discharge of stored Ca²⁺, a process generally termed Ca²⁺ oscillations (Prince and Berridge 1973; Woods et al. 1986). Like Ca²⁺ action potentials, these all-or-none discharges of Ca²⁺ represent a form of excitable behavior of the intracellular Ca²⁺ release signaling mechanism. However, because it is not possible to easily monitor and control the transmembrane chemical and biophysical parameters, as is the case for excitable plasma membrane behavior, it has been more difficult to fully understand the basic mechanisms by which these Ca²⁺ oscillations arise. Thus, although the question has been exhaustively studied for well over twenty years, there is still uncertainty and controversy over the underlying processes that give rise to Ca²⁺ oscillations. A number of reviews have discussed these issues at some length (Berridge and Galione 1988; Rink and Jacob 1989; Berridge 1990; Petersen and Wakui 1990; Berridge 1991; Cuthbertson and Cobbold 1991; Meyer and Stryer 1991; Hellman et al. 1992; Tepikin and Petersen 1992; Thomas et al. 1992; Dupont and Goldbeter 1993; Keizer 1993; Sneyd et al. 1994; Li et al. 1995; Thomas et al. 1996; Shuttleworth 1999; Lewis 2003; Dupont et al. 2007). In the current treatment, we have chosen to focus on two important aspects of Ca²⁺ oscillations. First, we review the available evidence for various computational models of Ca²⁺ oscillations that employ a quantitative approach to validate or repudiate specific mechanisms. Second, we consider the interrelationship between Ca²⁺ oscillations and plasma membrane Ca²⁺ influx mechanisms, with the view that we may learn more of the physiological function that these intracellular discharges of Ca²⁺ provide.