Universal Evolution of CKM Matrix Elements

We derive the two-loop evolution equations for the Cabibbo-Kobayashi-Maskawa matrix. We show that to leading order in the mass and CKM hierarchies the scaling of the mixings $|V_{ub}|^2$, $|V_{cb}|^2$, $|V_{td}|^2$, $|V_{ts}|^2$ and of the rephase-invariant CP-violating parameter $J$ is universal to all orders in perturbation theory. In leading order the other CKM elements do not scale. Imposing the constraint $\lambda _b=\lambda _{\tau}$ at the GUT scale determines the CKM scaling factor to be $\simeq 0.58$ in the MSSM.Comment: 17 pages + 2 figures not included (available upon request), revised version fixes discrepancy between S and S^{1/2}, no other changes, MAD/PH/72

A Generalization of the Convex Kakeya Problem

Given a set of line segments in the plane, not necessarily finite, what is a convex region of smallest area that contains a translate of each input segment? This question can be seen as a generalization of Kakeya's problem of finding a convex region of smallest area such that a needle can be rotated through 360 degrees within this region. We show that there is always an optimal region that is a triangle, and we give an optimal \Theta(n log n)-time algorithm to compute such a triangle for a given set of n segments. We also show that, if the goal is to minimize the perimeter of the region instead of its area, then placing the segments with their midpoint at the origin and taking their convex hull results in an optimal solution. Finally, we show that for any compact convex figure G, the smallest enclosing disk of G is a smallest-perimeter region containing a translate of every rotated copy of G.Comment: 14 pages, 9 figure

Spin-Polarized STM for a Kondo adatom

We investigate the bias dependence of the tunneling conductance between a spin-polarized (SP) scanning tunneling microscope (STM) tip and the surface conduction states of a normal metal with a Kondo adatom. Quantum interference between tip-host metal and tip-adatom-host metal conduction paths is studied in the full range of the Fano parameter $q$. The spin-polarized STM gives rise to a splitting of the Kondo peak and asymmetry in the zero-bias anomaly depending on the lateral tip-adatom distance. For increasing lateral distances, the Kondo peak-splitting shows a strong suppression and the spin-polarized conductance exhibits the standard Fano-Kondo profile.Comment: new version with improved discussion. added one figure. 12 pages (one-column) + 5 figure

The ORF59 DNA polymerase processivity factor homologs of Old World primate RV2 rhadinoviruses are highly conserved nuclear antigens expressed in differentiated epithelium in infected macaques

Background ORF59 DNA polymerase processivity factor of the human rhadinovirus, Kaposi's sarcoma-associated herpesvirus (KSHV), is required for efficient copying of the genome during virus replication. KSHV ORF59 is antigenic in the infected host and is used as a marker for virus activation and replication. Results We cloned, sequenced and expressed the genes encoding related ORF59 proteins from the RV1 rhadinovirus homologs of KSHV from chimpanzee (PtrRV1) and three species of macaques (RFHVMm, RFHVMn and RFHVMf), and have compared them with ORF59 proteins obtained from members of the more distantly-related RV2 rhadinovirus lineage infecting the same non-human primate species (PtrRV2, RRV, MneRV2, and MfaRV2, respectively). We found that ORF59 homologs of the RV1 and RV2 Old World primate rhadinoviruses are highly conserved with distinct phylogenetic clustering of the two rhadinovirus lineages. RV1 and RV2 ORF59 C-terminal domains exhibit a strong lineage-specific conservation. Rabbit antiserum was developed against a C-terminal polypeptide that is highly conserved between the macaque RV2 ORF59 sequences. This anti-serum showed strong reactivity towards ORF59 encoded by the macaque RV2 rhadinoviruses, RRV (rhesus) and MneRV2 (pig-tail), with no cross reaction to human or macaque RV1 ORF59 proteins. Using this antiserum and RT-qPCR, we determined that RRV ORF59 is expressed early after permissive infection of both rhesus primary fetal fibroblasts and African green monkey kidney epithelial cells (Vero) in vitro. RRV- and MneRV2-infected foci showed strong nuclear expression of ORF59 that correlated with production of infectious progeny virus. Immunohistochemical studies of an MneRV2-infected macaque revealed strong nuclear expression of ORF59 in infected cells within the differentiating layer of epidermis corroborating previous observations that differentiated epithelial cells are permissive for replication of KSHV-like rhadinoviruses Conclusion The ORF59 DNA polymerase processivity factor homologs of the Old World primate RV1 and RV2 rhadinovirus lineages are phylogenetically distinct yet demonstrate similar expression and localization characteristics that correlate with their use as lineage-specific markers for permissive infection and virus replication. These studies will aid in the characterization of virus activation from latency to the replicative state, an important step for understanding the biology and transmission of rhadinoviruses, such as KSHV

Surface Defect Dynamics in Organic–Inorganic Hybrid Perovskites: From Mechanism to Interfacial Properties

Organic–inorganic hybrid perovskites (OHPs) have garnered much attention among the photovoltaic and light-emitting diode research community due to their excellent optoelectronic properties and low-cost fabrication. Defects in perovskites have been proposed to affect device efficiency and stability and to have a potential role in enabling ion migration. In this study, the dynamic behavior and electronic properties of intrinsic defects in CH3NH3PbBr3 (MAPbBr3) were explored at the atomic scale. We use scanning tunneling microscopy to show unambiguously the occurrence of vacancy-assisted transport of individual ions as well as the existence of vacancy defect clusters at the OHP surface. We combine these observations with density functional theory (DFT) calculations to identify the mechanisms for this ion motion and show that ion transport energy barriers, as well as transport mechanisms, at the surface depend on crystal direction. DFT calculations also reveal that vacancy defect clusters can significantly modify the local work function of the perovskite surface, which is then expected to alter interfacial charge transport in a device. Our work provides a microscopic insight into the mechanism of ion migration in OHPs and also delivers the useful information for device improvement from the perspective of interface engineering

Effect of Stress on Viral–Bacterial Synergy in Bovine Respiratory Disease: Novel Mechanisms to Regulate Inflammation

The severity of bovine respiratory infections has been linked to a variety of factors, including environmental and nutritional changes, transportation, and social reorganization of weaned calves. Fatal respiratory infections, however, usually occur when a primary viral infection compromises host defences and enhances the severity of a secondary bacterial infection. This viral–bacterial synergy can occur by a number of different mechanisms and disease challenge models have been developed to analyse host responses during these respiratory infections. A primary bovine herpesvirus-1 (BHV-1) respiratory infection followed by a secondary challenge with Mannheimia haemolytica results in fatal bovine respiratory disease (BRD) and host responses to these two pathogens have been studied extensively. We used this disease model to demonstrate that stress significantly altered the viral–bacterial synergy resulting in fatal BRD. Functional genomic analysis revealed that BHV-1 infection enhanced toll-like receptors (TLR) expression and increased pro-inflammatory responses which contribute to the severity of a Mannheimia haemolytica infection. TLRs play a critical role in detecting bacterial infections and inducing pro-inflammatory responses. It is difficult to understand, however, how stress-induced corticosteroids could enhance this form of viral–bacterial synergy. Nuclear translocation of the glucocorticoid receptor activates cell signalling pathways which inhibit both TLR signalling and pro-inflammatory responses. The apparent conundrum between stress-induced corticosteroids and enhanced BRD susceptibility is discussed in terms of present data and previous investigations of stress and respiratory disease