Molecular dynamics simulation of polyacrylamide adsorption on calcite

In poorly consolidated carbonate rock reservoirs, solids production risk, which can lead to increased environmental waste, can be mitigated by injecting formation-strengthening chemicals. Classical atomistic molecular dynamics (MD) simulation is employed to model the interaction of polyacrylamide-based polymer additives with a calcite structure, which is the main component of carbonate formations. Amongst the possible calcite crystal planes employed as surrogates of reservoir rocks, the (1 0 4) plane is shown to be the most suitable surrogate for assessing the interactions with chemicals due to its stability and more realistic representation of carbonate structure. The molecular conformation and binding energies of pure polyacrylamide (PAM), hydrolysed polyacrylamide in neutral form (HPAM), hydrolysed polyacrylamide with 33% charge density (HPAM 33%) and sulfonated polyacrylamide with 33% charge density (SPAM 33%) are assessed to determine the adsorption characteristics onto calcite surfaces. An adsorption-free energy analysis, using an enhanced umbrella sampling method, is applied to evaluate the chemical adsorption performance. The interaction energy analysis shows that the polyacrylamide-based polymers display favourable interactions with the calcite structure. This is attributed to the electrostatic attraction between the amide and carboxyl functional groups with the calcite. Simulations confirm that HPAM33% has a lower free energy than other polymers, presumably due to the presence of the acrylate monomer in ionised form. The superior chemical adsorption performance of HPAM33% agrees with Atomic Force Microscopy experiments reported herein

Requirements for Membrane Attack Complex Formation and Anaphylatoxins Binding to Collagen-Activated Platelets

The activation of complement during platelet activation is incompletely understood.We sought to explore the formation of C5b-9 and anaphylatoxins binding to collagen-activated platelets.C5b-9, anaphylatoxins C3a, C4a and C5a, and anaphylatoxin receptors C3aR1 and C5aR were measured by flow cytometry and/or confocal microscopy. Platelet microparticles were quantified by flow cytometry, and their C5b-9 content was determined by western blot analyses. In all experiments, sodium citrate was used for blood anticoagulation.C5b-9 rapidly formed on the platelet surface following activation with collagen, TRAP, ADP or A23187, but was surprisingly restricted to a subset of platelets (1 to 15%) independently of P-selectin or phosphatidylserine exposure. Following collagen activation, C5b-9-positive platelets in thrombi were found associated with collagen fibres. C5b-9 formation was obliterated by Mg(2+)-EGTA and significantly reduced by the thrombin inhibitor hirudin (-37%, p<0.05), but was unaffected by chondroitinase, compstatin, SCH79797 (PAR-1 inhibitor), or in the PRP of a MBL-deficient donor. Compstatin and Mg(2+)-EGTA, but not hirudin, SCH79797 or chondroitinase, inhibited the formation of collagen-induced microparticles (-71% and -44%, respectively, p<0.04). These microparticles contained greater amounts of C5b-9 compared with the other agonists. Platelet activation by collagen or convulxin resulted in the strong binding of anaphylatoxins and the exposure of receptors C3aR1 and C5aR (CD88) on their surface.C5b-9 formation on collagen-activated platelets is i) partially controlled by thrombin, ii) restricted to a subset of platelets, and iii) can occur without P-selectin expression or phosphatidylserine exposure. Activated platelets bind anaphylatoxins on their surface and express C3a and C5a receptors, which may contribute to the localization of inflammatory processes during thrombosis

Displayed correlation between gene expression profiles and submicroscopic alterations in response to cetuximab, gefitinib and EGF in human colon cancer cell lines

Background: EGFR is frequently overexpressed in colon cancer. We characterized HT-29 and Caco-2, human colon cancer cell lines, untreated and treated with cetuximab or gefitinib alone and in combination with EGF. Methods: Cell growth was determined using a variation on the MTT assay. Cell-cycle analysis was conducted by flow cytometry. Immunohistochemistry was performed to evaluate EGFR expression and scanning electron microscopy (SEM) evidenced the ultrastructural morphology. Gene expression profiling was performed using hybridization of the microarray Ocimum Pan Human 40 K array A. Results: Caco-2 and HT-29 were respectively 66.25 and 59.24 % in G0/G1. They maintained this level of cell cycle distribution after treatment, suggesting a predominantly differentiated state. Treatment of Caco-2 with EGF or the two EGFR inhibitors produced a significant reduction in their viability. SEM clearly showed morphological cellular transformations in the direction of cellular death in both cell lines treated with EGFR inhibitors. HT-29 and Caco-2 displayed an important reduction of the microvilli (which also lose their erect position in Caco-2), possibly invalidating microvilli absorption function. HT-29 treated with cetuximab lost their boundary contacts and showed filipodi; when treated with gefitinib, they showed some vesicles: generally membrane reshaping is evident. Both cell lines showed a similar behavior in terms of on/off switched genes upon treatment with cetuximab. The gefitinib global gene expression pattern was different for the 2 cell lines; gefitinib treatment induced more changes, but directly correlated with EGF treatment. In cetuximab or gefitinib plus EGF treatments there was possible summation of the morphological effects: cells seemed more weakly affected by the transformation towards apoptosis. The genes appeared to be less stimulated than for single drug cases. Conclusion: This is the first study to have systematically investigated the effect of cetuximab or gefitinib, alone and in combination with EGF, on human colon cancer cell lines. The EGFR inhibitors have a weaker effect in the presence of EGF that binds EGFR. Cetuximab treatment showed an expression pattern that inversely correlates with EGF treatment. We found interesting cytomorphological features closely relating to gene expression profile. Both drugs have an effect on differentiation towards cellular death

Resistência a antifúngicos de Candida tropicalis isoladas no Estado do Ceará Antifungal resistance of Candida tropicalis isolated in the State of Ceará

Neste estudo, foi avaliada a resistência a drogas antifúngicas em 51 cepas de Candida tropicalis isoladas de amostras clínicas no Estado do Ceará, Brasil. Resistência antifúngica foi um evento raro no nosso estudo e foi restrita a 3 (5,9%) das cepas de Candida tropicalis, que exibiram resistência a fluconazol e itraconazol.<br>In this study, the resistance to antifungal drugs was investigated among 51 strains of Candida tropicalis isolated from clinical samples in the State of Ceará, Brazil. Antifungal resistance was a rare finding in our study and was restricted to three (5.9%) of the strains of Candida tropicalis. These exhibited resistance to both fluconazole and itraconazole