Quantum Symmetries and Strong Haagerup Inequalities

In this paper, we consider families of operators $\{x_r\}_{r \in \Lambda}$ in a tracial C$^\ast$-probability space $(\mathcal A, \phi)$, whose joint $\ast$-distribution is invariant under free complexification and the action of the hyperoctahedral quantum groups $\{H_n^+\}_{n \in \N}$. We prove a strong form of Haagerup's inequality for the non-self-adjoint operator algebra $\mathcal B$ generated by $\{x_r\}_{r \in \Lambda}$, which generalizes the strong Haagerup inequalities for $\ast$-free R-diagonal families obtained by Kemp-Speicher \cite{KeSp}. As an application of our result, we show that $\mathcal B$ always has the metric approximation property (MAP). We also apply our techniques to study the reduced C$^\ast$-algebra of the free unitary quantum group $U_n^+$. We show that the non-self-adjoint subalgebra $\mathcal B_n$ generated by the matrix elements of the fundamental corepresentation of $U_n^+$ has the MAP. Additionally, we prove a strong Haagerup inequality for $\mathcal B_n$, which improves on the estimates given by Vergnioux's property RD \cite{Ve}

Developmental arrest of T cells in RpL22-deficient mice is dependent upon multiple p53 effectors

available in PMC 2012 July 15alpha beta and gamma delta lineage T cells are thought to arise from a common CD4–CD8– progenitor in the thymus. However, the molecular pathways controlling fate selection and maturation of these two lineages remain poorly understood. We demonstrated recently that a ubiquitously expressed ribosomal protein, Rpl22, is selectively required for the development of alpha beta lineage T cells. Germline ablation of Rpl22 impairs development of alpha beta lineage, but not gamma delta lineage, T cells through activation of a p53-dependent checkpoint. In this study, we investigate the downstream effectors used by p53 to impair T cell development. We found that many p53 targets were induced in Rpl22−/− thymocytes, including miR-34a, PUMA, p21waf, Bax, and Noxa. Notably, the proapoptotic factor Bim, while not a direct p53 target, was also strongly induced in Rpl22−/− T cells. Gain-of-function analysis indicated that overexpression of miR-34a caused a developmental arrest reminiscent of that induced by p53 in Rpl22-deficient T cells; however, only a few p53 targets alleviated developmental arrest when individually ablated by gene targeting or knockdown. Co-elimination of PUMA and Bim resulted in a nearly complete restoration of development of Rpl22−/− thymocytes, indicating that p53-mediated arrest is enforced principally through effects on cell survival. Surprisingly, co-elimination of the primary p53 regulators of cell cycle arrest (p21waf) and apoptosis (PUMA) actually abrogated the partial rescue caused by loss of PUMA alone, suggesting that the G1 checkpoint protein p21[superscript waf] facilitates thymocyte development in some contexts.National Institutes of Health (U.S.) ( (NIH) Grant R01AI073920)National Institutes of Health (U.S.) (NIH Core Grant P01CA06927)National Institutes of Health (U.S.) ( (NIH) Grant R21CA141194)National Institutes of Health (U.S.) ( NIH Center Grant P30-DK-50306)Pennsylvania (appropriation)Fox Chase Cancer Center (NIH Postdoctoral Training Grant T32 CA00903534)Fox Chase Cancer Center (NIH Postdoctoral Training Grant F32 AI089077-01A1

Non-Gaussianities in N-flation

We compute non-Gaussianities in N-flation, a string motivated model of assisted inflation with quadratic, separable potentials and masses given by the Marcenko-Pastur distribution. After estimating parameters characterizing the bi- and trispectrum in the horizon crossing approximation, we focus on the non-linearity parameter $f_{NL}$, a measure of the bispectrum; we compute its magnitude for narrow and broad spreads of masses, including the evolution of modes after horizon crossing. We identify additional contributions due to said evolution and show that they are suppressed as long as the fields are evolving slowly. This renders $\mathcal{N}$-flation indistinguishable from simple single-field models in this regime. Larger non-Gaussianities are expected to arise for fields that start to evolve faster, and we suggest an analytic technique to estimate their contribution. However, such fast roll during inflation is not expected in N-flation, leaving (p)re-heating as the main additional candidate for generating non-Gaussianities.Comment: 27 pages, 4 figures, extended references to match version accepted in JCA

Suicide Seasonality: Complex Demodulation as a Novel Approach in Epidemiologic Analysis

Seasonality of suicides is well-known and nearly ubiquitous, but recent evidence showed inconsistent patterns of decreasing or increasing seasonality in different countries. Furthermore, strength of seasonality was hypothesized to be associated with suicide prevalence. This study aimed at pointing out methodological difficulties in examining changes in suicide seasonality. METHODODOLOGY/PRINCIPAL FINDINGS: The present study examines the hypothesis of decreasing seasonality with a superior method that allows continuous modeling of seasonality. Suicides in Austria (1970-2008, N = 67,741) were analyzed with complex demodulation, a local (point-in-time specific) version of harmonic analysis. This avoids the need to arbitrarily split the time series, as is common practice in the field of suicide seasonality research, and facilitates incorporating the association with suicide prevalence. Regression models were used to assess time trends and association of amplitude and absolute suicide numbers. Results showed that strength of seasonality was associated with absolute suicide numbers, and that strength of seasonality was stable during the study period when this association was taken into account.Continuous modeling of suicide seasonality with complex demodulation avoids spurious findings that can result when time series are segmented and analyzed piecewise or when the association with suicide prevalence is disregarded

Transcriptomic, proteomic and metabolomic analysis of UV-B signaling in maize

<p>Abstract</p> <p>Background</p> <p>Under normal solar fluence, UV-B damages macromolecules, but it also elicits physiological acclimation and developmental changes in plants. Excess UV-B decreases crop yield. Using a treatment twice solar fluence, we focus on discovering signals produced in UV-B-irradiated maize leaves that translate to systemic changes in shielded leaves and immature ears.</p> <p>Results</p> <p>Using transcriptome and proteomic profiling, we tracked the kinetics of transcript and protein alterations in exposed and shielded organs over 6 h. In parallel, metabolic profiling identified candidate signaling molecules based on rapid increase in irradiated leaves and increased levels in shielded organs; pathways associated with the synthesis, sequestration, or degradation of some of these potential signal molecules were UV-B-responsive. Exposure of just the top leaf substantially alters the transcriptomes of both irradiated and shielded organs, with greater changes as additional leaves are irradiated. Some phenylpropanoid pathway genes are expressed only in irradiated leaves, reflected in accumulation of pathway sunscreen molecules. Most protein changes detected occur quickly: approximately 92% of the proteins in leaves and 73% in immature ears changed after 4 h UV-B were altered by a 1 h UV-B treatment.</p> <p>Conclusions</p> <p>There were significant transcriptome, proteomic, and metabolomic changes under all conditions studied in both shielded and irradiated organs. A dramatic decrease in transcript diversity in irradiated and shielded leaves occurs between 0 h and 1 h, demonstrating the susceptibility of plants to short term UV-B spikes as during ozone depletion. Immature maize ears are highly responsive to canopy leaf exposure to UV-B.</p

Histoplasma capsulatum Encodes a Dipeptidyl Peptidase Active against the Mammalian Immunoregulatory Peptide, Substance P

The pathogenic fungus Histoplasma capsulatum secretes dipeptidyl peptidase (Dpp) IV enzyme activity and has two putative DPPIV homologs (HcDPPIVA and HcDPPIVB). We previously showed that HcDPPIVB is the gene responsible for the majority of secreted DppIV activity in H. capsulatum culture supernatant, while we could not detect any functional contribution from HcDPPIVA. In order to determine whether HcDPPIVA encodes a functional DppIV enzyme, we expressed HcDPPIVA in Pichia pastoris and purified the recombinant protein. The recombinant enzyme cleaved synthetic DppIV substrates and had similar biochemical properties to other described DppIV enzymes, with temperature and pH optima of 42°C and 8, respectively. Recombinant HcDppIVA cleaved the host immunoregulatory peptide substance P, indicating the enzyme has the potential to affect the immune response during infection. Expression of HcDPPIVA under heterologous regulatory sequences in H. capsulatum resulted in increased secreted DppIV activity, indicating that the encoded protein can be expressed and secreted by its native organism. However, HcDPPIVA was not required for virulence in a murine model of histoplasmosis. This work reports a fungal enzyme that can function to cleave the immunomodulatory host peptide substance P

Effect of CD26/dipeptidyl peptidase IV on Jurkat sensitivity to G2/M arrest induced by topoisomerase II inhibitors

CD26/dipeptidyl peptidase IV (DPPIV) is a surface antigen with multiple functions, including a role in T-cell activation and the development of certain human cancers. We previously demonstrated that CD26/DPPIV enhanced sensitivity of Jurkat cells to doxorubicin. We now show that expression of CD26/DPPIV enhanced sensitivity of CD26 Jurkat transfectants to G2–M arrest mediated by the antineoplastic agent etoposide. The increased sensitivity to etoposide-induced G2–M arrest was associated with disruption of cell cycle-related events, including hyperphosphorylation of p34cdc2 kinase, change in cdc25C expression and phosphorylation, and alteration in cyclin B1 expression. CD26/DPPIV-associated enhancement of doxorubicin and etoposide-induced G2–M arrest was also observed in serum-free media, suggesting an effect of CD26 on cell-derived processes rather than serum-derived factors. Importantly, our work elucidated a potential mechanism for the enhanced susceptibility of CD26-expressing Jurkat cells to the topoisomerase II inhibitors by demonstrating that CD26/DPPIV surface expression was associated with increased topoisomerase II α levels and enhanced enzyme activity. Besides being the first to show a functional association between the multifaceted molecule CD26 and the key cellular protein topoisomerase II α, our studies provide additional evidence of a potential role for CD26 in the treatment of selected malignancies

Hydrothermal dolomitization of basinal deposits controlled by a synsedimentary fault system in Triassic extensional setting, Hungary

Dolomitization of relatively thick carbonate successions occurs via an effective fluid circulation mechanism, since the replacement process requires a large amount of Mg-rich fluid interacting with the CaCO3 precursor. In the western end of the Neotethys, fault-controlled extensional basins developed during the Late Triassic spreading stage. In the Buda Hills and Danube-East blocks, distinct parts of silica and organic matter-rich slope and basinal deposits are dolomitized. Petrographic, geochemical, and fluid inclusion data distinguished two dolomite types: (1) finely to medium crystalline and (2) medium to coarsely crystalline. They commonly co-occur and show a gradual transition. Both exhibit breccia fabric under microscope. Dolomite texture reveals that the breccia fabric is not inherited from the precursor carbonates but was formed during the dolomitization process and under the influence of repeated seismic shocks. Dolomitization within the slope and basinal succession as well as within the breccia zones of the underlying basement block is interpreted as being related to fluid originated from the detachment zone and channelled along synsedimentary normal faults. The proposed conceptual model of dolomitization suggests that pervasive dolomitization occurred not only within and near the fault zones. Permeable beds have channelled the fluid towards the basin centre where the fluid was capable of partial dolomitization. The fluid inclusion data, compared with vitrinite reflectance and maturation data of organic matter, suggest that the ascending fluid was likely hydrothermal which cooled down via mixing with marine-derived pore fluid. Thermal gradient is considered as a potential driving force for fluid flow