Parton Energy Loss and the Generalized Jet Transport Coefficient

We revisit radiative parton energy loss in deeply inelastic scattering (DIS) off a large nucleus within the perturbative QCD approach. We calculate the gluon radiation spectra induced by double parton scattering in DIS without collinear expansion in the transverse momentum of initial gluons as in the original high-twist approach. The final radiative gluon spectrum can be expressed in terms of the convolution of hard partonic parts and unintegrated or transverse momentum dependent (TMD) quark-gluon correlations. The TMD quark-gluon correlation can be factorized approximately as a product of initial quark distribution and TMD gluon distribution which can be used to define the generalized or TMD jet transport coefficient. Under the static scattering center and soft radiative gluon approximation, we recover the result by Gylassy-Levai-Vitev (GLV) in the first order of the opacity expansion. The difference as a result of the soft radiative gluon approximation is investigated numerically under the static scattering center approximation.Comment: 33 pages in RevTeX with 30 figures, final version appeared in PRD with additional typos correcte

Evaluation of Fluvial Geomorphic Responses to the Removal of Dams with the Consideration of Hydrological Uncertainty: a Case Study in Shihgang Dam

Source: ICHE Conference Archive - https://mdi-de.baw.de/icheArchive

The unique rapid variabilities of the iron Kα\alpha line profiles in NGC 4151

We present a detailed analysis of the iron K$\alpha$ line variabilities in NGC 4151 by using long ASCA observation data obtained in May 1995. Despite the relatively small amplitude variations in the continuum flux, the iron K$\alpha$ line flux and profile show dramatic variations. Particularly, the line profile changes from single peak to seeming double peaks and back in time scales of a few 10$^4$ sec. The seemingly double-peaked profiles can be well interpreted as line emission from a Keplerian ring around a massive black hole. An absorption line at around 5.9 keV is also marginnaly detected. We discussed current Fe K line models, but none of them can well explain the observed line and continuum variations.Comment: 18 pages, latex, 3 figures, ApJ accepte

Mechanism of Polarization Fatigue in BiFeO3: the Role of Schottky Barrier

By using piezoelectric force microscopy and scanning Kelvin probe microscopy, we have investigated the domain evolution and space charge distribution in planar BiFeO3 capacitors with different electrodes. It is observed that charge injection at the film/electrode interface leads to domain pinning and polarization fatigue in BiFeO3. Furthermore, the Schottky barrier at the interface is crucial for the charge injection process. Lowering the Schottky barrier by using low work function metals as the electrodes can also improve the fatigue property of the device, similar to what oxide electrodes can achieve

DHX33 transcriptionally controls genes involved in the cell cycle

The RNA helicase DHX33 has been shown to be a critical regulator of cell proliferation and growth. However, the underlying mechanisms behind DHX33 function remain incompletely understood. We present original evidence in multiple cell lines that DHX33 transcriptionally controls the expression of genes involved in the cell cycle, notably cyclin, E2F1, cell division cycle (CDC), and minichromosome maintenance (MCM) genes. DHX33 physically associates with the promoters of these genes and controls the loading of active RNA polymerase II onto these promoters. DHX33 deficiency abrogates cell cycle progression and DNA replication and leads to cell apoptosis. In zebrafish, CRISPR-mediated knockout of DHX33 results in downregulation of cyclin A2, cyclin B2, cyclin D1, cyclin E2, cdc6, cdc20, E2F1, and MCM complexes in DHX33 knockout embryos. Additionally, we found the overexpression of DHX33 in a subset of non-small-cell lung cancers and in Ras-mutated human lung cancer cell lines. Forced reduction of DHX33 in these cancer cells abolished tumor formation in vivo. Our study demonstrates for the first time that DHX33 acts as a direct transcriptional regulator to promote cell cycle progression and plays an important role in driving cell proliferation during both embryo development and tumorigenesis