Attochirp-free High-order Harmonic Generation

A method is proposed for arbitrarily engineering the high-order harmonic generation phase achieved by shaping a laser pulse and employing xuv light or x rays for ionization. This renders the production of bandwidth-limited attosecond pulses possible while avoiding the use of filters for chirp compensation. By adding the first 8 Fourier components to a sinusoidal field of $10^{16}$W/cm$^2$, the bandwidth-limited emission of 8 as is shown to be possible from a Li$^{2+}$ gas. The scheme is extendable to the zs-scale

Nonredundant Roles for CD1d-restricted Natural Killer T Cells and Conventional CD4+ T Cells in the Induction of Immunoglobulin E Antibodies in Response to Interleukin 18 Treatment of Mice

Interleukin (IL)-18 synergizes with IL-12 to promote T helper cell (Th)1 responses. Somewhat paradoxically, IL-18 administration alone strongly induces immunoglobulin (Ig)E production and allergic inflammation, indicating a role for IL-18 in the generation of Th2 responses. The ability of IL-18 to induce IgE is dependent on CD4+ T cells, IL-4, and signal transducer and activator of transcription (stat)6. Here, we show that IL-18 fails to induce IgE both in CD1d−/− mice that lack natural killer T (NKT) cells and in class II−/− mice that lack conventional CD4+ T cells. However, class II−/− mice reconstituted with conventional CD4+ T cells show the capacity to produce IgE in response to IL-18. NKT cells express high levels of IL-18 receptor (R)α chain and produce significant amounts of IL-4, IL-9, and IL-13, and induce CD40 ligand expression in response to IL-2 and IL-18 stimulation in vitro. In contrast, conventional CD4+ T cells express low levels of IL-18Rα and poorly respond to IL-2 and IL-18. Nevertheless, conventional CD4+ T cells are essential for B cell IgE responses after the administration of IL-18. These findings indicate that NKT cells might be the major source of IL-4 in response to IL-18 administration and that conventional CD4+ T cells demonstrate their helper function in the presence of NKT cells

Differential Lipid Partitioning Between Adipocytes and Tissue Macrophages Modulates Macrophage Lipotoxicity and M2/M1 Polarization in Obese Mice

Objective: obesity-associated insulin resistance is characterized by a state of chronic, low-grade inflammation that is associated with the accumulation of M1 proinflammatory macrophages in adipose tissue. Although different evidence explains the mechanisms linking the expansion of adipose tissue and adipose tissue macrophage (ATM) polarization, in the current study we investigated the concept of lipid-induced toxicity as the pathogenic link that could explain the trigger of this response. Research design and methods: we addressed this question using isolated ATMs and adipocytes from genetic and diet-induced murine models of obesity. Through transcriptomic and lipidomic analysis, we created a model integrating transcript and lipid species networks simultaneously occurring in adipocytes and ATMs and their reversibility by thiazolidinedione treatment. Results: we show that polarization of ATMs is associated with lipid accumulation and the consequent formation of foam cell-like cells in adipose tissue. Our study reveals that early stages of adipose tissue expansion are characterized by M2-polarized ATMs and that progressive lipid accumulation within ATMs heralds the M1 polarization, a macrophage phenotype associated with severe obesity and insulin resistance. Furthermore, rosiglitazone treatment, which promotes redistribution of lipids toward adipocytes and extends the M2 ATM polarization state, prevents the lipid alterations associated with M1 ATM polarization. Conclusions:our data indicate that the M1 ATM polarization in obesity might be a macrophage-specific manifestation of a more general lipotoxic pathogenic mechanism. This indicates that strategies to optimize fat deposition and repartitioning toward adipocytes might improve insulin sensitivity by preventing ATM lipotoxicity and M1 polarization.</p

Wake up, wake up! It's me! It's my life! patient narratives on person-centeredness in the integrated care context: a qualitative study

Person-centered care emphasizes a holistic, humanistic approach that puts patients first, at the center of medical care. Person-centeredness is also considered a core element of integrated care. Yet typologies of integrated care mainly describe how patients fit within integrated services, rather than how services fit into the patient's world. Patient-centeredness has been commonly defined through physician's behaviors aimed at delivering patient-centered care. Yet, it is unclear how 'person-centeredness' is realized in integrated care through the patient voice. We aimed to explore patient narratives of person-centeredness in the integrated care context

Neutral Gauge Boson Contributions to the Dimuon Charge Asymmetry in B Decays

Recently, the D0 Collaboration measured the CP-violating like-sign dimuon charge asymmetry in neutral B decays, finding a 3.2sigma difference from the standard-model (SM) prediction. A non-SM charge asymmetry a_sl^s suggests a new-physics (NP) contribution to Bs-Bsbar mixing. In this case, in order to explain the measured value of a_sl^s within its 1sigma range, NP must be present in Gamma_12^s, the absorptive part of the mixing. In this paper, we examine whether such an explanation is possible in models with flavor-changing Z (ZFCNC) or Z' (Z'FCNC) gauge bosons. The models must also reproduce the measured values of the indirect CP asymmetry S_psi-phi in Bs -> J/psi phi, and Delta Gamma_s, the Bs-Bsbar width difference. We find that the ZFCNC model cannot reproduce the present measured values of S_psi-phi and a_sl^s within their 1sigma ranges. On the other hand, in the Z'FCNC model, the values of all three observables can be simultaneously reproduced.Comment: 18 pages, 7 figures, JHEP format. Some ZFCNC equations corrected, ZFCNC analysis redone, references added, conclusions unchange

New Physics in Bs -> J/psi phi: a General Analysis

Recently, the CDF and D0 collaborations measured indirect CP violation in Bs -> J/psi phi and found a hint of a signal. If taken at face value, this can be interpreted as a nonzero phase of Bs-Bsbar mixing (beta_s), in disagreement with the standard model, which predicts that beta_s ~= 0. In this paper, we argue that this analysis may be incomplete. In particular, there can be new physics (NP) in the bbar -> sbar c cbar decay. If so, the value of beta_s is different than for the case in which NP is assumed to be present only in the mixing. We have examined several models of NP and found that, indeed, there can be significant contributions to the decay. These effects are consistent with measurements in B -> J/psi K* and Bd -> J/psi Ks. Due to the NP in the decay, polarization-dependent indirect CP asymmetries and triple-product asymmetries are predicted in Bs -> J/psi phi.Comment: 28 pages, JHEP, no figures. Considerable changes made. Abstract and main text of paper modified to alter presentation. Appendix added. References added. Conclusions unchanged

An NLR paralog Pit2 generated from tandem duplication of Pit1 fine-tunes Pit1 localization and function

NLR family proteins act as intracellular receptors. Gene duplication amplifies the number of NLR genes, and subsequent mutations occasionally provide modifications to the second gene that benefits immunity. However, evolutionary processes after gene duplication and functional relationships between duplicated NLRs remain largely unclear. Here, we report that the rice NLR protein Pit1 is associated with its paralogue Pit2. The two are required for the resistance to rice blast fungus but have different functions: Pit1 induces cell death, while Pit2 competitively suppresses Pit1-mediated cell death. During evolution, the suppression of Pit1 by Pit2 was probably generated through positive selection on two fate-determining residues in the NB-ARC domain of Pit2, which account for functional differences between Pit1 and Pit2. Consequently, Pit2 lost its plasma membrane localization but acquired a new function to interfere with Pit1 in the cytosol. These findings illuminate the evolutionary trajectory of tandemly duplicated NLR genes after gene duplication

First study of \eta_c, \eta(1760) and X(1835) production via \eta'\pi^+\pi^- final states in two-photon collisions

The invariant mass spectrum of the \eta' \pi^+ \pi^- final state produced in two-photon collisions is obtained using a 673 fb^{-1} data sample collected in the vicinity of the \Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric-energy e^+e^- collider. We observe a clear signal of the \eta_c and measure its mass and width to be M(\eta_c)=(2982.7 +- 1.8(stat) +- 2.2(syst) +- 0.3(model)) MeV/c^2 and \Gamma(\eta_c) = (37.8^{+5.8}_{-5.3}(stat) +- 2.8(syst) +- 1.4(model)) MeV/c^2. The third error is an uncertainty due to possible interference between the \eta_c and a non-resonant component. We also report the first evidence for \eta(1760) decay to \eta' \pi^+ \pi^-; we find two solutions for its parameters, depending on the inclusion or not of the X(1835), whose existence is of marginal significance in our data. From a fit to the mass spectrum using coherent X(1835) and \eta(1760) resonant amplitudes, we set a 90% confidence level upper limit on the product \Gamma_{\gamma\gamma} \BR (\eta' \pi^+ \pi^-) for the X(1835).Comment: 13 pages, 7 figures, submitted to PR

Measurements of time-dependent CP asymmetries in B→D∗∓π±B \to D^{*\mp} \pi^{\pm} decays using a partial reconstruction technique

We report results on time-dependent CP asymmetries in $B \to D^{*\mp}\pi^{\pm}$ decays based on a data sample containing 657 {\times} $10^6$ $B\bar{B}$ pairs collected with the Belle detector at the KEKB asymmetric-energy $e^+ e^-$ collider at the $\Upsilon(4S)$ resonance. We use a partial reconstruction technique, wherein signal $B \to D^{*\mp}\pi^{\pm}$ events are identified using information only from the fast pion from the B decay and the slow pion from the subsequent decay of the $D^{*\mp}$, where the former (latter) corresponds to $D^{*+} (D^{*-})$ final states. We obtain CP violation parameters $S^+ = +0.061 \pm 0.018(\mathrm{stat}) \pm 0.012(\mathrm{syst})$ and $S^- = +0.031 \pm 0.019(\mathrm{stat}) \pm 0.015(\mathrm{syst})$.Comment: 8 pages, 5 figures, 2 tables, submitted to Physical Review D (RC