BCS and BEC p-wave pairing in Bose-Fermi gases

The pairing of fermionic atoms in a mixture of atomic fermion and boson gases at zero temperature is investigated. The attractive interaction between fermions, that can be induced by density fluctuations of the bosonic background, can give rise to a superfluid phase in the Fermi component of the mixture. The atoms of both species are assumed to be in only one internal state, so that the pairing of fermions is effective only in odd-l channels. No assumption about the value of the ratio between the Fermi velocity and the sound velocity in the Bose gas is made in the derivation of the energy gap equation. The gap equation is solved without any particular "ansatz" for the pairing field or the effective interaction. The p-wave superfluidity is studied in detail. By increasing the strength and/or decreasing the range of the effective interaction a transition of the fermion pairing regime, from the Bardeen-Cooper-Schrieffer state to a system of tightly bound couples can be realized. These composite bosons behave as a weakly-interacting Bose-Einstein condensate.Comment: 14 pages, 6 eps-figures. To be published in European Physical Journal

Preferential binding to elk-1 by sle-associated il10 risk allele upregulates il10 expression

Immunoregulatory cytokine interleukin-10 (IL-10) is elevated in sera from patients with systemic lupus erythematosus (SLE) correlating with disease activity. The established association of IL10 with SLE and other autoimmune diseases led us to fine map causal variant(s) and to explore underlying mechanisms. We assessed 19 tag SNPs, covering the IL10 gene cluster including IL19, IL20 and IL24, for association with SLE in 15,533 case and control subjects from four ancestries. The previously reported IL10 variant, rs3024505 located at 1 kb downstream of IL10, exhibited the strongest association signal and was confirmed for association with SLE in European American (EA) (P = 2.7×10−8, OR = 1.30), but not in non-EA ancestries. SNP imputation conducted in EA dataset identified three additional SLE-associated SNPs tagged by rs3024505 (rs3122605, rs3024493 and rs3024495 located at 9.2 kb upstream, intron 3 and 4 of IL10, respectively), and SLE-risk alleles of these SNPs were dose-dependently associated with elevated levels of IL10 mRNA in PBMCs and circulating IL-10 protein in SLE patients and controls. Using nuclear extracts of peripheral blood cells from SLE patients for electrophoretic mobility shift assays, we identified specific binding of transcription factor Elk-1 to oligodeoxynucleotides containing the risk (G) allele of rs3122605, suggesting rs3122605 as the most likely causal variant regulating IL10 expression. Elk-1 is known to be activated by phosphorylation and nuclear localization to induce transcription. Of interest, phosphorylated Elk-1 (p-Elk-1) detected only in nuclear extracts of SLE PBMCs appeared to increase with disease activity. Co-expression levels of p-Elk-1 and IL-10 were elevated in SLE T, B cells and monocytes, associated with increased disease activity in SLE B cells, and were best downregulated by ERK inhibitor. Taken together, our data suggest that preferential binding of activated Elk-1 to the IL10 rs3122605-G allele upregulates IL10 expression and confers increased risk for SLE in European Americans

Association of genetic variants in complement factor H and factor H-related genes with systemic lupus erythematosus susceptibility

Systemic lupus erythematosus (SLE), a complex polygenic autoimmune disease, is associated with increased complement activation. Variants of genes encoding complement regulator factor H (CFH) and five CFH-related proteins (CFHR1-CFHR5) within the chromosome 1q32 locus linked to SLE, have been associated with multiple human diseases and may contribute to dysregulated complement activation predisposing to SLE. We assessed 60 SNPs covering the CFH-CFHRs region for association with SLE in 15,864 case-control subjects derived from four ethnic groups. Significant allelic associations with SLE were detected in European Americans (EA) and African Americans (AA), which could be attributed to an intronic CFH SNP (rs6677604, in intron 11, Pmeta = 6.6×10-8, OR = 1.18) and an intergenic SNP between CFHR1 and CFHR4 (rs16840639, Pmeta = 2.9×10-7, OR = 1.17) rather than to previously identified disease-associated CFH exonic SNPs, including I62V, Y402H, A474A, and D936E. In addition, allelic association of rs6677604 with SLE was subsequently confirmed in Asians (AS). Haplotype analysis revealed that the underlying causal variant, tagged by rs6677604 and rs16840639, was localized to a ~146 kb block extending from intron 9 of CFH to downstream of CFHR1. Within this block, the deletion of CFHR3 and CFHR1 (CFHR3-1Δ), a likely causal variant measured using multiplex ligation-dependent probe amplification, was tagged by rs6677604 in EA and AS and rs16840639 in AA, respectively. Deduced from genotypic associations of tag SNPs in EA, AA, and AS, homozygous deletion of CFHR3-1Δ (Pmeta = 3.2×10-7, OR = 1.47) conferred a higher risk of SLE than heterozygous deletion (Pmeta = 3.5×10-4, OR = 1.14). These results suggested that the CFHR3-1Δ deletion within the SLE-associated block, but not the previously described exonic SNPs of CFH, might contribute to the development of SLE in EA, AA, and AS, providing new insights into the role of complement regulators in the pathogenesis of SLE

TMEFF2 Is a PDGF-AA Binding Protein with Methylation-Associated Gene Silencing in Multiple Cancer Types Including Glioma

BACKGROUND: TMEFF2 is a protein containing a single EGF-like domain and two follistatin-like modules. The biological function of TMEFF2 remains unclear with conflicting reports suggesting both a positive and a negative association between TMEFF2 expression and human cancers. METHODOLOGY/PRINCIPAL FINDINGS: Here we report that the extracellular domain of TMEFF2 interacts with PDGF-AA. This interaction requires the amino terminal region of the extracellular domain containing the follistatin modules and cannot be mediated by the EGF-like domain alone. Furthermore, the extracellular domain of TMEFF2 interferes with PDGF-AA-stimulated fibroblast proliferation in a dose-dependent manner. TMEFF2 expression is downregulated in human brain cancers and is negatively correlated with PDGF-AA expression. Suppressed expression of TMEFF2 is associated with its hypermethylation in several human tumor types, including glioblastoma and cancers of ovarian, rectal, colon and lung origins. Analysis of glioma subtypes indicates that TMEFF2 hypermethylation and decreased expression are associated with a subset of non-Proneural gliomas that do not display CpG island methylator phentoype. CONCLUSIONS/SIGNIFICANCE: These data provide the first evidence that TMEFF2 can function to regulate PDGF signaling and that it is hypermethylated and downregulated in glioma and several other cancers, thereby suggesting an important role for this protein in the etiology of human cancers

Understanding How University Students Use Perceptions of Consent, Wantedness, and Pleasure in Labeling Rape.

While the lack of consent is the only determining factor in considering whether a situation is rape or not, there is sufficient evidence that participants conflate wantedness with consent and pleasurableness with wantedness. Understanding how people appraise sexual scenarios may form the basis to develop appropriate educational packages. We conducted two large-scale qualitative studies in two UK universities in which participants read vignettes describing sexual encounters that were consensual or not, wanted or unwanted and pleasurable or not pleasurable. Participants provided free-text responses as to whether they perceived the scenarios to be rape or not and why they made these judgments. The second study replicated the results of the first and included a condition where participants imagined themselves as either the subject or initiator of the sexual encounter. The results indicate that a significant portion of our participants held attitudes reflecting rape myths and tended to blame the victim. Participants used distancing language when imagining themselves in the initiator condition. Participants indicated that they felt there were degrees of how much a scenario reflected rape rather than it simply being a dichotomy (rape or not). Such results indicate a lack of understanding of consent and rape and highlight avenues of potential educational materials for schools, universities or jurors

Characterization of RNA degradosome from E. coli with mutant polynucleotide phosphorylase

The RNA degradosome is a bacterial protein machine devoted to RNA turnover. Degradosomes and related complexes have been described in Escherichia coli and other prokaryotes as well as in eukaryotes. The integral components of the E. coli RNA degradosome include the endoribonuclease RNase E, the phosphorolytic exoribonuclease polynucleotide phosphorylase (PNPase), the DEAD-box helicase RhlB, and enolase, a glycolytic enzyme commonly implicated in an apparently unrelated process. It is believed that the degradosome coordinates the endo- and exonucleolytic activities of RNase E and PNPase, respectively, whereas the ATP-consuming RhlB helicase would promote the unwinding of double stranded RNA, thus facilitating progression of PNPase through RNA secondary structures. Many questions are still open on the composition, molecular interactions, assembly pathway, mechanism of action, and physiological significance of this molecular machine. To get further insights into the structure and function of this protein complex, we investigated on the properties of RNA degradosomes associated with mutant PNPases with single aminoacid substitutions in different domains and exhibiting different phenotypic traits. The mutant proteins were expressed from plasmid vectors in a PNPase-null E. coli mutant together with a FLAG-tagged RNase E. Degradosomes were then purified by FLAG-affinity chromatography and assayed for the RhlB-promoted degradation of a structured RNA substrate (malE-malF intergenic region) in the presence of ATP (1,2,3). None of mutations tested impaired assembly of PNPase with RNase E and, for most mutants, the RNA-degrading ability of the degradosome correlated with the phosphorolytic activity of the mutant PNPase. An exception was Pnp-E81D, which harbors a single aminoacid substitution on the outer side of the trimerization interface. Although in crude extracts neither phosphorolytic activity nor RNA binding appeared to be impaired, the mutant was defective in autogenous regulation. The RNA degradosome containing Pnp-E81D was unable to degrade the structured RNA substrate. This seemed to correlate with a lower abundance of the RhlB RNA helicase. It thus appears that PNPase participates in the assembly of RhlB in the degradosome and/or in the control of the RNA helicase activity. In addition, these data suggest the participation of the RhlB RNA helicase in PNPase autogenous regulation. References 1. Miczak, A., Kaberdin, V.R., Wei, C.L., and Lin-Chao, S. Proteins associated with RNase E in a multicomponent ribonucleolytic complex. Proc. Natl. Acad. Sci. USA 93 (1996) 3865\u20133869. 2. Regonesi, M. E., Del Favero, M., Basilico, F., Briani, F., Benazzi, L., Tortora, P., Mauri, P., and Deh\uf2, G. (2006) Analysis of the Escherichia coli RNA degradosome composition by a proteomic approach. Biochimie 88:151-161. 3. Py, B., Higgins, C. F., Krisch, H. M., and Carpousis, A. J. (1996) A DEAD-box RNA helicase in the Escherichia coli RNA degradosome. Nature 381:169-172

Characterization of RNA degradosome from E. coli with mutant polynucleotide phosphorylase

The RNA degradosome is a bacterial protein machine devoted to RNA turnover. Degradosomes and related complexes have been described in Escherichia coli and other prokaryotes as well as in eukaryotes. The integral components of the E. coli RNA degradosome include the endoribonuclease RNase E, the phosphorolytic exoribonuclease polynucleotide phosphorylase (PNPase), the DEAD-box helicase RhlB, and enolase, a glycolytic enzyme commonly implicated in an apparently unrelated process. Many questions are still open on the composition, molecular interactions, assembly pathway, mechanism of action, and physiological significance of this molecular machine. To get further insights into the structure and function of this protein complex, we investigated on the properties of RNA degradosomes purified from pnp mutant strains expressing PNPases with single aminoacid substitutions in different domains. None of mutations tested impaired assembly of PNPase with RNase E and, for most mutants, the RNA-degrading ability of the degradosome correlated with the phosphorolytic activity of the mutant PNPase. An exception was Pnp-E81D, which harbors a single aminoacid substitution on the outer side of the trimerization interface. Although in crude extracts neither phosphorolytic activity nor RNA binding appeared to be impaired, the mutant was defective in autogenous regulation. The RNA degradosome containing Pnp-E81D was unable to degrade a structured RNA substrate. This seemed to correlate with a lower abundance of the RhlB RNA helicase. It thus appears that PNPase participates in the assembly of RhlB in the degradosome and/or in the control of the RNA helicase activity. In addition, these data suggest the participation of the RhlB RNA helicase in PNPase autogenous regulation