Influence of solvent quality on polymer solutions: a Monte Carlo study of bulk and interfacial properties

The effect of solvent quality on dilute and semi-dilute regimes of polymers in solution is studied by means of Monte Carlo simulations. The equation of state, adsorptions near a hard wall, wall-polymer surface tension and effective depletion potentials are all calculated as a function of concentration and solvent quality. We find important differences between polymers in good and theta solvents. In the dilute regime, the physical properties for polymers in a theta solvent closely resemble those of ideal polymers. In the semi-dilute regime, however, significant differences are found.Comment: 10 pages, 13 figure

Excitons and high-order optical transitions in individual carbon nanotubes

We examine the excitonic nature of high-lying optical transitions in single-walled carbon nanotubes by means of Rayleigh scattering spectroscopy. A careful analysis of the principal transitions of individual semiconducting and metallic nanotubes reveals that in both cases the lineshape is consistent with an excitonic model, but not one of free-carriers. For semiconducting species, side-bands are observed at ~200 meV above the third and fourth optical transitions. These features are ascribed to exciton-phonon bound states. Such side-bands are not apparent for metallic nanotubes,as expected from the reduced strength of excitonic interactions in these systems

Coarse-graining strategies in polymer solutions

We review a coarse-graining strategy (multiblob approach) for polymer solutions in which groups of monomers are mapped onto a single atom (a blob) and effective blob-blob interactions are obtained by requiring the coarse-grained model to reproduce some coarse-grained features of the zero-density isolated-chain structure. By tuning the level of coarse graining, i.e. the number of monomers to be mapped onto a single blob, the model should be adequate to explore the semidilute regime above the collapse transition, since in this case the monomer density is very small if chains are long enough. The implementation of these ideas has been previously based on a transferability hypothesis, which was not completely tested against full-monomer results (Pierleoni et al., J. Chem. Phys, 127, 171102 (2007)). We study different models proposed in the past and we compare their predictions to full-monomer results for the chain structure and the thermodynamics in the range of polymer volume fractions \Phi between 0 and 8. We find that the transferability assumption has a limited predictive power if a thermodynamically consistent model is required. We introduce a new tetramer model parametrized in such a way to reproduce not only zero-density intramolecular and intermolecular two-body probabilities, but also some intramolecular three-body and four-body distributions. We find that such a model correctly predicts three-chain effects, the structure and the thermodynamics up to \Phi ~ 2, a range considerably larger than that obtained with previous simpler models using zero-density potentials. Our results show the correctness of the ideas behind the multiblob approach but also that more work is needed to understand how to develop models with more effective monomers which would allow us to explore the semidilute regime at larger chain volume fractions.Comment: 33 pages, 19 figures, submitted to Soft Matte

Recovery from hind limb ischemia is less effective in type 2 than in type 1 diabetic mice: Roles of endothelial nitric oxide synthase and endothelial progenitor cells

ObjectiveWe sought to directly compare the effects of type 1 and type 2 diabetes on postischemic neovascularization and evaluate the mechanisms underlying differences between these groups. We tested the hypothesis that type 2 diabetic mice have a greater reduction in endothelial nitric oxide synthase (eNOS) expression, a greater increase in oxidative stress, and reduced arteriogenesis and angiogenesis, resulting in less complete blood flow recovery than type 1 diabetic mice after induction of hind limb ischemia.MethodsHind limb ischemia was generated by femoral artery excision in streptozotocin-treated mice (model of type 1 diabetes), in Leprdb/db mice (model of type 2 diabetes), and in control (C57BL/6) mice. Dependent variables included eNOS expression and markers of arteriogenesis, angiogenesis, and oxidative stress.ResultsPostischemia recovery of hind limb perfusion was significantly less in type 2 than in type 1 diabetic mice; however, neither group demonstrated a significant increase in collateral artery diameter or collateral artery angioscore in the ischemic hind limb. The capillary/myofiber ratio in the gastrocnemius muscle decreased in response to ischemia in control or type 1 diabetic mice but remained the same in type 2 diabetic mice. Gastrocnemius muscle eNOS expression was lower in type 1 and 2 diabetic mice than in control mice. This expression decreased after induction of ischemia in type 2 but not in type 1 diabetic mice. The percentage of endothelial progenitor cells (EPC) in the peripheral blood failed to increase in either diabetic group after induction of ischemia, whereas this variable significantly increased in the control group in response to ischemia. EPC eNOS expression decreased after induction of ischemia in type 1 but not in type 2 diabetic mice. EPC nitrotyrosine accumulation increased after induction of ischemia in type 2 but not in type 1 diabetic mice. EPC migration in response to vascular endothelial growth factor was reduced in type 1 and type 2 diabetic mice vs control mice. EPC incorporation into tubular structures was less effective in type 2 diabetic mice. Extensive fatty infiltration was present in ischemic muscle of type 2 but not in type 1 diabetic mice.ConclusionType 2 diabetic mice displayed a significantly less effective response to hind limb ischemia than type 1 diabetic mice.Clinical RelevanceDiabetes is important in the pathogenesis of peripheral artery disease. The present study demonstrates that the vascular response to acute hind limb ischemia is dependent on the type of diabetes present. Type 2 diabetic mice (Leprdb/db) demonstrated significantly less effective blood flow recovery than type 1 diabetic mice (streptozotocin-induced). Moreover, the differences between diabetic groups appeared contingent, at least in part, on differences in endothelial nitric oxide, oxidant stress, and endothelial progenitor cell function between the two diabetic groups. Although direct extrapolation of animal data to the human experience must be made with caution, these findings indicate that the type of diabetes present, and not just the presence of diabetes per se, may be important in the initiation of progression of peripheral artery disease

Type 2 Diabetes-Induced Hematopoietic Stem Cell Oxidant Stress Attenuates the Differentiation, Skews M1/M2 Specification of Monocytes/Macrophages and Delays Wound Healing in db/db Mice

Rationale: After recruitment to wounds, monocytes differentiate into macrophages which play a central role in all stages of wound healing. Wound healing is significantly delayed in type 2 diabetics. Although accumulating evidence suggests that delayed wound healing in type 2 diabetics is related to macrophages specification into M1/M2 phenotypes, the mechanism remains unknown. Objective: This study tested the hypothesis that type 2 diabetes induces hematopoietic stem cells (HSCs) oxidant stress that reduces their differentiation towards monocytes and skews the specification of M1/M2 phenotype, thereby causing delayed wound healing. Methods and Results: HSCs were sorted from bone marrow of WT and db/db type 2 diabetic mice. DCF staining showed significant oxidant accumulation in HSCs from db/db mice which was reversed by the antioxidant, N-acetylcysteine (NAC). Bone marrow monocyte concentration (FACS analysis of cell surface markers f4/80, cd14 and cd115) was significantly lower in db/db mice than in WT mice. NAC also reversed the reduced differentiation towards monocytes. Wound closure rate was significantly delayed in db/db mice. Macrophages were isolated from wounds and their concentration and M1/M2 phenotype were quantified by flow cytometry. During the inflammatory phase of wound healing, macrophage concentration was decreased and the proportion of M1 macrophages was lower in db/db mice than in WT mice. During new tissue formation phase, macrophage concentration was decreased and the proportion of M2 macrophage was lower, but M1 macrophage was higher in db/db mice than in WT mice. During tissue remodeling phase, macrophage concentration was increased and M1 macrophage remained higher in db/db mice, but no difference was observed in the proportion of M2 macrophages. The reduced differentiation of HSCs towards monocytes and the delayed wound closure phenotype of db/db mice could be transferred to WT mice by transplanting db/db HSCs into lethally irradiated WT mice. Conclusion: Type 2 diabetes-induced HSC oxidant stress impairs HSC differentiation towards monocytes, skews the M1/M2 specification of macrophages and thereby accounts for the delayed wound healing. Type 2 diabetes-induced HSC oxidant stress may be a heretofore unrecognized critical regulator of dysinflammation in type 2 diabetic

Frequent expansion of Plasmodium vivax Duffy Binding Protein in Ethiopia and its epidemiological significance.

Plasmodium vivax invasion of human erythrocytes depends on the Duffy Binding Protein (PvDBP) which interacts with the Duffy antigen. PvDBP copy number has been recently shown to vary between P. vivax isolates in Sub-Saharan Africa. However, the extent of PvDBP copy number variation, the type of PvDBP multiplications, as well as its significance across broad samples are still unclear. We determined the prevalence and type of PvDBP duplications, as well as PvDBP copy number variation among 178 Ethiopian P. vivax isolates using a PCR-based diagnostic method, a novel quantitative real-time PCR assay and whole genome sequencing. For the 145 symptomatic samples, PvDBP duplications were detected in 95 isolates, of which 81 had the Cambodian and 14 Malagasy-type PvDBP duplications. PvDBP varied from 1 to >4 copies. Isolates with multiple PvDBP copies were found to be higher in symptomatic than asymptomatic infections. For the 33 asymptomatic samples, PvDBP was detected with two copies in two of the isolates, and both were the Cambodian-type PvDBP duplication. PvDBP copy number in Duffy-negative heterozygotes was not significantly different from that in Duffy-positives, providing no support for the hypothesis that increased copy number is a specific association with Duffy-negativity, although the number of Duffy-negatives was small and further sampling is required to test this association thoroughly

The human telomerase RNA gene (hTERC) is regulated during carcinogenesis but is not dependent on DNA methylation

Telomerase, the ribonucleoprotein complex involved in telomere maintenance, is composed of two main components: hTERT and hTERC. hTERT seems to be the rate-limiting factor for telomerase activity, although hTERC expression was also shown to correlate to a certain extent with telomerase reactivation. To determine whether the absence of hTERC expression could be the consequence of DNA methylation, we quantified hTERC RNA in 60 human samples (19 telomerase-negative normal tissues, nine telomerase-positive and 22 telomerase-negative tumor tissues, eight telomerase-positive and two telomerase-negative cell lines) using a quantitative dot blot on RT-PCR products. Most of the normal tissues did not express hTERC whereas, in telomerase-positive cell lines and in telomerase-positive tumor tissues, a strong up-regulation was observed, suggesting that hTERC transcription is up-regulated during tumorigenesis. The two telomerase-negative cell lines did not express hTERC. In a series of 22 telomerase-negative soft tissue sarcomas (STS), half did not express hTERC at all, or only weakly, whereas a wide range of expression was observed in the other half. As methylation might be involved in hTERC silencing, we examined the methylation pattern in all samples by direct sequencing and methylation-specific single stand conformation analysis after bisulfite modification. hTERC methylation was never observed, neither in normal nor in tumor tissues. Furthermore, there was no correlation between hTERC expression and proliferation, telomere length or hTERT expression in telomerase-negative STS. In contrast, three of eight telomerase-positive cell lines and the two telomerasenegative cell lines were found to be hypermethylated, suggesting that the methylation observed may occur during cell line establishment. In conclusion, this study shows that hTERC expression is indeed regulated during carcinogenesis, but this regulation is unlikely to depend on hTERC methylation, cell proliferation rate, telomere length or hTERT expressio