Multivariable Scaling for the Anomalous Hall Effect

We derive a general scaling relation for the anomalous Hall effect in ferromagnetic metals involving multiple competing scattering mechanisms, described by a quadratic hypersurface in the space spanned by the partial resistivities. We also present experimental findings, which show strong deviation from previously found scaling forms when different scattering mechanism compete in strength but can be nicely explained by our theory

Hot Spine Loops and the Nature of a Late-Phase Solar Flare

The fan-spine magnetic topology is believed to be responsible for many curious features in solar explosive events. A spine field line links distinct flux domains, but direct observation of such feature has been rare. Here we report a unique event observed by the Solar Dynamic Observatory where a set of hot coronal loops (over 10 MK) connected to a quasi-circular chromospheric ribbon at one end and a remote brightening at the other. Magnetic field extrapolation suggests these loops are partly tracer of the evolving spine field line. Continuous slipping- and null-point-type reconnections were likely at work, energizing the loop plasma and transferring magnetic flux within and across the fan quasi-separatrix layer. We argue that the initial reconnection is of the "breakout" type, which then transitioned to a more violent flare reconnection with an eruption from the fan dome. Significant magnetic field changes are expected and indeed ensued. This event also features an extreme-ultraviolet (EUV) late phase, i.e. a delayed secondary emission peak in warm EUV lines (about 2-7 MK). We show that this peak comes from the cooling of large post-reconnection loops beside and above the compact fan, a direct product of eruption in such topological settings. The long cooling time of the large arcades contributes to the long delay; additional heating may also be required. Our result demonstrates the critical nature of cross-scale magnetic coupling - topological change in a sub-system may lead to explosions on a much larger scale.Comment: Accepted for publication in ApJ. Animations linked from pd

Hormad1 mutation disrupts synaptonemal complex formation, recombination, and chromosome segregation in mammalian meiosis

Meiosis is unique to germ cells and essential for reproduction. During the first meiotic division, homologous chromosomes pair, recombine, and form chiasmata. The homologues connect via axial elements and numerous transverse filaments to form the synaptonemal complex. The synaptonemal complex is a critical component for chromosome pairing, segregation, and recombination. We previously identified a novel germ cell-specific HORMA domain encoding gene, Hormad1, a member of the synaptonemal complex and a mammalian counterpart to the yeast meiotic HORMA domain protein Hop1. Hormad1 is essential for mammalian gametogenesis as knockout male and female mice are infertile. Hormad1 deficient (Hormad1-/-) testes exhibit meiotic arrest in the early pachytene stage, and synaptonemal complexes cannot be visualized by electron microscopy. Hormad1 deficiency does not affect localization of other synaptonemal complex proteins, SYCP2 and SYCP3, but disrupts homologous chromosome pairing. Double stranded break formation and early recombination events are disrupted in Hormad1-/- testes and ovaries as shown by the drastic decrease in the γH2AX, DMC1, RAD51, and RPA foci. HORMAD1 co-localizes with cH2AX to the sex body during pachytene. BRCA1, ATR, and γH2AX co-localize to the sex body and participate in meiotic sex chromosome inactivation and transcriptional silencing. Hormad1 deficiency abolishes γH2AX, ATR, and BRCA1 localization to the sex chromosomes and causes transcriptional de-repression on the X chromosome. Unlike testes, Hormad1-/- ovaries have seemingly normal ovarian folliculogenesis after puberty. However, embryos generated from Hormad1-/- oocytes are hyper- and hypodiploid at the 2 cell and 8 cell stage, and they arrest at the blastocyst stage. HORMAD1 is therefore a critical component of the synaptonemal complex that affects synapsis, recombination, and meiotic sex chromosome inactivation and transcriptional silencing. © 2010 Shin et al

Induction chemotherapy for squamous cell carcinomas of the oral cavity: A cumulative meta-analysis

Induction chemotherapy (ICT) is a controversial treatment for head and neck squamous cell carcinomas (HNSCC). Despite numerous randomized controlled trials (RCTs), a majority do not have enough statistical power alone to conclude ICT’s treatment value among oral squamous carcinoma patients (OSCC) since many addressed HNSCC as one entity instead of by specific subtypes. By performing a systematic review and cumulative meta-analysis, we aim to determine the benefits of ICT in OSCC therapy. A literature search identified for RCTs comparing OSCC patients who received ICT against those without. Log-hazard ratio, and relative risk were used for comparison. Heterogeneity was determined using the I2 statistic package. The primary endpoint was overall survival (OS), followed by disease-free survival (DFS), locoregional recurrence (LRR) and distant metastasis (DM) as secondary endpoints. RESULTS: 27 randomized trials were included for analysis (n = 2872 patients). The shortest median follow-up was 15 months whereas the longest was 11.5 years. ICT does not improve OS (HR = 0.947, 95% CI 0.85–1.05, p = 0.318), DFS (RR = 1.05, 95% CI 0.92–1.21, p = 0.462) and DM (RR = 0.626, CI 95% 0.361–1.086, p = 0.096) compared to locoregional treatment alone. However, there was a significant improvement to LRR (RR = 0.778, 95% CI 0.622–0.972, p = 0.027). There is no evidence ICT improves survival outcomes for OSCC patients. However, ICT reduces locoregional recurrence of OSCC, which may need further verification.preprin

Drosophila Bruce Can Potently Suppress Rpr- and Grim-Dependent but Not Hid-Dependent Cell Death

Bruce is a large protein (530 kDa) that contains an N-terminal baculovirus IAP repeat (BIR) and a C-terminal ubiquitin conjugation domain (E2) 1, 2. BRUCE upregulation occurs in some cancers and contributes to the resistance of these cells to DNA-damaging chemotherapeutic drugs [2]. However, it is still unknown whether Bruce inhibits apoptosis directly or instead plays some other more indirect role in mediating chemoresistance, perhaps by promoting drug export, decreasing the efficacy of DNA damage-dependent cell death signaling, or by promoting DNA repair. Here, we demonstrate, using gain-of-function and deletion alleles, that Drosophila Bruce (dBruce) can potently inhibit cell death induced by the essential Drosophila cell death activators Reaper (Rpr) and Grim but not Head involution defective (Hid). The dBruce BIR domain is not sufficient for this activity, and the E2 domain is likely required. dBruce does not promote Rpr or Grim degradation directly, but its antiapoptotic actions do require that their N termini, required for interaction with DIAP1 BIR2, be intact. dBruce does not block the activity of the apical cell death caspase Dronc or the proapoptotic Bcl-2 family member Debcl/Drob-1/dBorg-1/Dbok. Together, these results argue that dBruce can regulate cell death at a novel point

Constraints on B--->pi,K transition form factors from exclusive semileptonic D-meson decays

According to the heavy-quark flavour symmetry, the $B\to \pi, K$ transition form factors could be related to the corresponding ones of D-meson decays near the zero recoil point. With the recent precisely measured exclusive semileptonic decays $D \to \pi \ell \nu$ and $D\to K \ell \nu$, we perform a phenomenological study of $B \to \pi, K$ transition form factors based on this symmetry. Using BK, BZ and Series Expansion parameterizations of the form factor slope, we extrapolate $B \to \pi, K$ transition form factors from $q^{2}_{max}$ to $q^{2}=0$. It is found that, although being consistent with each other within error bars, the central values of our results for $B \to \pi, K$ form factors at $q^2=0$, $f_+^{B\to \pi, K}(0)$, are much smaller than predictions of the QCD light-cone sum rules, but are in good agreements with the ones extracted from hadronic B-meson decays within the SCET framework. Moreover, smaller form factors are also favored by the QCD factorization approach for hadronic B-meson decays.Comment: 19 pages, no figure, 5 table

Does the 2D Hubbard Model Really Show d-Wave Superconductivity?

Some issues concerning the question if the two-dimensional Hubbard model really show d-wave superconductivity are briefly discussed.Comment: Revtex, no figure

Energy Momentum Pseudo-Tensor of Relic Gravitational Wave in Expanding Universe

We study the energy-momentum pseudo-tensor of gravitational wave, and examine the one introduced by Landau-Lifshitz for a general gravitational field and the effective one recently used in literature. In short wavelength limit after Brill-Hartle average, both lead to the same gauge invariant stress tensor of gravitational wave. For relic gravitational waves in the expanding universe, we examine two forms of pressure, $p_{gw}$ and $\mathcal{P}_{gw}$, and trace the origin of their difference to a coupling between gravitational waves and the background matter. The difference is shown to be negligibly small for most of cosmic expansion stages starting from inflation. We demonstrate that the wave equation is equivalent to the energy conservation equation using the pressure $\mathcal{P}_{gw}$ that includes the mentioned coupling.Comment: 15 pages, no figure, Accepted by PR