QCD's equation of state from Dyson-Schwinger equations

In this contribution, we summarize a truncation-independent method to compute the equation of state within nonperturbative functional approaches. After demonstrating its viability, the method is applied to solutions obtained from a set of truncated Dyson-Schwinger equations for the quark and gluon propagators of (2+1)-flavor QCD to obtain thermodynamic quantities across the phase diagram of strong-interaction matter.Comment: 6 pages, 2 figures; contribution to the proceedings of the FAIR next generation scientists workshop (FAIRNESS), 7th edition, 23-27 May 2022, Paralia (Pieria), Greec

Sulindac sulfide reverses aberrant self-renewal of progenitor cells induced by the AML-associated fusion proteins PML/RARalpha and PLZF/RARalpha

Chromosomal translocations can lead to the formation of chimeric genes encoding fusion proteins such as PML/RARalpha, PLZF/RARalpha, and AML-1/ETO, which are able to induce and maintain acute myeloid leukemia (AML). One key mechanism in leukemogenesis is increased self renewal of leukemic stem cells via aberrant activation of the Wnt signaling pathway. Either X-RAR, PML/RARalpha and PLZF/RARalpha or AML-1/ETO activate Wnt signaling by upregulating gamma-catenin and beta-catenin. In a prospective study, a lower risk of leukemia was observed with aspirin use, which is consistent with numerous studies reporting an inverse association of aspirin with other cancers. Furthermore, a reduction in leukemia risk was associated with use of non-steroidal anti-inflammatory drug (NSAID), where the effects on AML risk was FAB subtype-specific. To better investigate whether NSAID treatment is effective, we used Sulindac Sulfide in X-RARalpha-positive progenitor cell models. Sulindac Sulfide (SSi) is a derivative of Sulindac, a NSAID known to inactivate Wnt signaling. We found that SSi downregulated both beta-catenin and gamma-catenin in X-RARalpha-expressing cells and reversed the leukemic phenotype by reducing stem cell capacity and increasing differentiation potential in X-RARalpha-positive HSCs. The data presented herein show that SSi inhibits the leukemic cell growth as well as hematopoietic progenitors cells (HPCs) expressing PML/RARalpha, and it indicates that Sulindac is a valid molecular therapeutic approach that should be further validated using in vivo leukemia models and in clinical settings

Prokaryotic Diversity and Community Patterns in Antarctic Continental Shelf Sponges

Marine sponges (Phylum Porifera) are globally distributed within marine and freshwater ecosystems. In addition, sponges host dense and diverse prokaryotic communities, which are potential sources of novel bioactive metabolites and other complex compounds. Those sponge-derived natural products can span a broad spectrum of bioactivities, from antibacterial and antifungal to antitumor and antiviral compounds. However, most analyses concerning sponge-associated prokaryotes have mainly focused on conveniently accessible relatively shallow sampling locations for sponges. Hence, knowledge of community composition, host-relatedness and biotechnological potential of prokaryotic associations in temperate and cold-water sponges from greater depths (mesophotic to mesopelagic zones) is still scarce. Therefore, we analyzed the prokaryotic community diversity of four phylogenetically divergent sponge taxa from mesophotic to mesopelagic depths of Antarctic shelf at different depths and locations in the region of the South Shetland Islands using 16S rRNA gene amplicon-based sequencing. In addition, we predicted functional profiles applying Tax4Fun from metagenomic 16S rRNA gene data to estimate their biotechnological capability and possible roles as sources of novel bioactive compounds. We found indications that cold and deep-water sponges exhibit host-specific prokaryotic communities, despite different sampling sites and depths. Functional prediction analysis suggests that the associated prokaryotes may enhance the roles of sponges in biodegradation processes of xenobiotics and their involvement in the biosynthesis of secondary metabolites

Sulindac Sulfide Reverses Aberrant Self-Renewal of Progenitor Cells Induced by the AML-Associated Fusion Proteins PML/RARα and PLZF/RARα

Chromosomal translocations can lead to the formation of chimeric genes encoding fusion proteins such as PML/RARα, PLZF/RARα, and AML-1/ETO, which are able to induce and maintain acute myeloid leukemia (AML). One key mechanism in leukemogenesis is increased self renewal of leukemic stem cells via aberrant activation of the Wnt signaling pathway. Either X-RAR, PML/RARα and PLZF/RARα or AML-1/ETO activate Wnt signaling by upregulating γ-catenin and β-catenin. In a prospective study, a lower risk of leukemia was observed with aspirin use, which is consistent with numerous studies reporting an inverse association of aspirin with other cancers. Furthermore, a reduction in leukemia risk was associated with use of non-steroidal anti-inflammatory drug (NSAID), where the effects on AML risk was FAB subtype-specific. To better investigate whether NSAID treatment is effective, we used Sulindac Sulfide in X-RARα-positive progenitor cell models. Sulindac Sulfide (SSi) is a derivative of Sulindac, a NSAID known to inactivate Wnt signaling. We found that SSi downregulated both β-catenin and γ-catenin in X-RARα-expressing cells and reversed the leukemic phenotype by reducing stem cell capacity and increasing differentiation potential in X-RARα-positive HSCs. The data presented herein show that SSi inhibits the leukemic cell growth as well as hematopoietic progenitors cells (HPCs) expressing PML/RARα, and it indicates that Sulindac is a valid molecular therapeutic approach that should be further validated using in vivo leukemia models and in clinical settings

Weak Glycolipid Binding of a Microdomain-Tracer Peptide Correlates with Aggregation and Slow Diffusion on Cell Membranes

10.1371/journal.pone.0051222PLoS ONE712

Phase diagram of the Polyakov–Nambu–Jona-Lasinio approach for finite chemical potentials

International audienceWe extend the SU(3) (Polyakov)–Nambu–Jona-Lasinio in two ways: We introduce the next-to-leading-order contribution (in Nc) in the partition function. This contribution contains explicit mesonic terms. We introduce a coupling between the gluon field and the quark degrees of freedom, which goes beyond a simple rescaling of the critical temperature. With both these improvements, we can reproduce, for vanishing chemical potentials, the lattice results for the thermal properties of a strongly interacting system like pressure, energy density, entropy density, interaction measure, and the speed of sound. Also, the expansion parameter toward small but finite chemical potentials agrees with the lattice results. Extending the calculations to finite chemical potentials (which does not require any new parameter), we find a first-order phase transition up to a critical end point of TCEP=110MeV and μq=320MeV. We calculate the mass of mesons and baryons as a function of temperature and chemical potential and the transition between the hadronic and the chirally restored phase. These calculations provide an equation of state in the whole T,μ plane an essential ingredient for dynamical calculations of ultrarelativistic heavy-ion collisions but also for the physics of neutron stars and neutron star collisions

β(2) integrins are required for skin homing of primed T cells but not for priming naive T cells

β(2) integrins are of critical importance for leukocyte extravasation through vascular endothelia and for T cell activation. To elucidate the role of β(2) integrins in T cell–mediated immune responses, allergic contact dermatitis (ACD), irritant dermatitis, and delayed-type hypersensitivity (DTH) were assessed in mice lacking the β(2) integrin subunit, CD18. ACD and DTH responses, but not edema formation, were severely suppressed in CD18(–/–) mice. Extravasation of CD18(–/–) T cells into eczematous skin lesions was greatly impaired, whereas migration of Langerhans cell precursors and dendritic cells was normal in CD18(–/–) mice. CD18(–/–)lymph nodes (LNs) contained an abnormal population of CD3(–)CD44(high) lymphocytes and showed evidence of widespread T cell activation. T cells from regional LNs of sensitized CD18(–/–) mice proliferated in response to hapten challenge, and subcutaneous injection of sensitized syngeneic LN cells directly into ears of hapten-challenged naive recipients restored the defective ACD in CD18(–/–) mice, suggesting that CD18 is not required for priming of naive T cells but is indispensable for T cell extravasation. Thus, a dysfunction of T cells, in addition to granulocytes, may contribute to the pathophysiology of leukocyte adhesion deficiency type I, which arises from mutations in the human CD18 gene