AGK Cutting Rules and Multiple Scattering in Hadronic Collisions

We discuss the AGK rules for the exchange of an arbitrary number of reggeized gluons in perturbative QCD in the high energy limit. Results include the cancellation of corrections to single jet and double jet inclusive cross sections, both for hard and soft rescattering contributions.Comment: 31 pages, latex, 20 figure

A molecular mechanism for the water-hydroxyl balance during wetting of TiO2

We show that the formation of the wetting layer and the experimentally observed continuous shift of the H2O-OH balance towards molecular water at increasing coverage on a TiO2(110) surface can be rationalized on a molecular level. The mechanism is based on the initial formation of stable hydroxyl pairs, a repulsive interaction between these pairs and an attractive interaction with respect to water molecules. The experimental data are obtained by synchrotron radiation photoelectron spectroscopy and interpreted with the aid of density functional theory calculations and Monte Carlo simulations

Toxicological and analytical assessment of e-cigarette refill components on airway epithelia

© 2016, Science Reviews 2000 Ltd. All rights reserved.There are over 2.6 million users of e-cigarettes in the United Kingdom alone as they have been promoted as a safer alternative to traditional cigarettes. The addition of flavours and aromas has also proven to be popular with younger generations. In this review, we survey the range of studies in the short timeframe since e-cigarettes reached the market to draw attention to the health associated risks and benefits of their introduction. We complement this review with a case study reporting on the composition of selected e-cigarette refills with particular emphasis on the toxicological activity of its components on lung cells

Multiparton interactions and production of minijets in high energy hadronic collisions

We discuss the inclusive cross section to produce two minijets with a large separation in rapidity in high energy hadronic collisions. The contribution to the inclusive cross section from the exchange of a BFKL Pomeron is compared with the contribution from the exchange of two BFKL Pomerons, which is induced by the unitarization of the semi-hard interaction. The effect of the multiple exchange is studied both as a function of the azimuthal correlation and as a function of the transverse momentum of the observed minijets.Comment: TeX file, 20 pages, 4 figures available on reques

Combined transcriptome studies identify AFF3 as a mediator of the oncogenic effects of beta-catenin in adrenocortical carcinoma

Adrenocortical cancer (ACC) is a very aggressive tumor, and genomics studies demonstrate that the most frequent alterations of driver genes in these cancers activate the Wnt/beta-catenin signaling pathway. However, the adrenal-specific targets of oncogenic beta-catenin-mediating tumorigenesis have not being established. A combined transcriptomic analysis from two series of human tumors and the human ACC cell line H295R harboring a spontaneous beta-catenin activating mutation was done to identify the Wnt/beta-catenin targets. Seven genes were consistently identified in the three studies. Among these genes, we found that AFF3 mediates the oncogenic effects of beta-catenin in ACC. The Wnt response element site located at nucleotide position - 1408 of the AFF3 transcriptional start sites (TSS) mediates the regulation by the Wnt/beta-catenin signaling pathway. AFF3 silencing decreases cell proliferation and increases apoptosis in the ACC cell line H295R. AFF3 is located in nuclear speckles, which play an important role in RNA splicing. AFF3 overexpression in adrenocortical cells interferes with the organization and/or biogenesis of these nuclear speckles and alters the distribution of CDK9 and cyclin T1 such that they accumulate at the sites of AFF3/speckles. We demonstrate that AFF3 is a new target of Wnt/beta-catenin pathway involved in ACC, acting on transcription and RNA splicing

Combined transcriptome studies identify AFF3 as a mediator of the oncogenic effects of beta-catenin in adrenocortical carcinoma

Adrenocortical cancer (ACC) is a very aggressive tumor, and genomics studies demonstrate that the most frequent alterations of driver genes in these cancers activate the Wnt/beta-catenin signaling pathway. However, the adrenal-specific targets of oncogenic beta-catenin-mediating tumorigenesis have not being established. A combined transcriptomic analysis from two series of human tumors and the human ACC cell line H295R harboring a spontaneous beta-catenin activating mutation was done to identify the Wnt/beta-catenin targets. Seven genes were consistently identified in the three studies. Among these genes, we found that AFF3 mediates the oncogenic effects of beta-catenin in ACC. The Wnt response element site located at nucleotide position - 1408 of the AFF3 transcriptional start sites (TSS) mediates the regulation by the Wnt/beta-catenin signaling pathway. AFF3 silencing decreases cell proliferation and increases apoptosis in the ACC cell line H295R. AFF3 is located in nuclear speckles, which play an important role in RNA splicing. AFF3 overexpression in adrenocortical cells interferes with the organization and/or biogenesis of these nuclear speckles and alters the distribution of CDK9 and cyclin T1 such that they accumulate at the sites of AFF3/speckles. We demonstrate that AFF3 is a new target of Wnt/beta-catenin pathway involved in ACC, acting on transcription and RNA splicing

Synthesis of Densely Packaged, Ultrasmall Pt02Clusters within a Thioether-Functionalized MOF: Catalytic Activity in Industrial Reactions at Low Temperature

The gram\u2010scale synthesis, stabilization, and characterization of well\u2010defined ultrasmall subnanometric catalytic clusters on solids is a challenge. The chemical synthesis and X\u2010ray snapshots of Pt02 clusters, homogenously distributed and densely packaged within the channels of a metal\u2013organic framework, is presented. This hybrid material catalyzes efficiently, and even more importantly from an economic and environmental viewpoint, at low temperature (25 to 140\u2009\ub0C), energetically costly industrial reactions in the gas phase such as HCN production, CO2 methanation, and alkene hydrogenations. These results open the way for the design of precisely defined catalytically active ultrasmall metal clusters in solids for technically easier, cheaper, and dramatically less\u2010dangerous industrial reactions

Cushing's Syndrome and Fetal Features Resurgence in Adrenal Cortex–Specific Prkar1a Knockout Mice

Carney complex (CNC) is an inherited neoplasia syndrome with endocrine overactivity. Its most frequent endocrine manifestation is primary pigmented nodular adrenocortical disease (PPNAD), a bilateral adrenocortical hyperplasia causing pituitary-independent Cushing's syndrome. Inactivating mutations in PRKAR1A, a gene encoding the type 1 α-regulatory subunit (R1α) of the cAMP–dependent protein kinase (PKA) have been found in 80% of CNC patients with Cushing's syndrome. To demonstrate the implication of R1α loss in the initiation and development of PPNAD, we generated mice lacking Prkar1a specifically in the adrenal cortex (AdKO). AdKO mice develop pituitary-independent Cushing's syndrome with increased PKA activity. This leads to autonomous steroidogenic genes expression and deregulated adreno-cortical cells differentiation, increased proliferation and resistance to apoptosis. Unexpectedly, R1α loss results in improper maintenance and centrifugal expansion of cortisol-producing fetal adrenocortical cells with concomitant regression of adult cortex. Our data provide the first in vivo evidence that loss of R1α is sufficient to induce autonomous adrenal hyper-activity and bilateral hyperplasia, both observed in human PPNAD. Furthermore, this model demonstrates that deregulated PKA activity favors the emergence of a new cell population potentially arising from the fetal adrenal, giving new insight into the mechanisms leading to PPNAD

An experimental study of cathodic protection for chloride contaminated reinforced concrete

Cathodic protection (CP) is being increasingly used on reinforced concrete structures to protect steel reinforcing bars from corrosion in aggressive conditions. Due to the complexity of environmental conditions, the design specifications in national and international standards are still open to discussion to achieve both sufficient and efficient protection for reinforced concrete structures in engineering practices. This paper reports an experimental research to investigate the influence of chloride content on concrete resistivity, rebar corrosion rate and the performance of CP operation using different current densities. It aims to understand the correlation between the chloride content and concrete resistivity together with the CP current requirement, and to investigate the precision of the CP design criteria in standards

Aldo Keto Reductase 1B7 and Prostaglandin F2α Are Regulators of Adrenal Endocrine Functions

Prostaglandin F2α (PGF2α), represses ovarian steroidogenesis and initiates parturition in mammals but its impact on adrenal gland is unknown. Prostaglandins biosynthesis depends on the sequential action of upstream cyclooxygenases (COX) and terminal synthases but no PGF2α synthases (PGFS) were functionally identified in mammalian cells. In vitro, the most efficient mammalian PGFS belong to aldo-keto reductase 1B (AKR1B) family. The adrenal gland is a major site of AKR1B expression in both human (AKR1B1) and mouse (AKR1B3, AKR1B7). Thus, we examined the PGF2α biosynthetic pathway and its functional impact on both cortical and medullary zones. Both compartments produced PGF2α but expressed different biosynthetic isozymes. In chromaffin cells, PGF2α secretion appeared constitutive and correlated to continuous expression of COX1 and AKR1B3. In steroidogenic cells, PGF2α secretion was stimulated by adrenocorticotropic hormone (ACTH) and correlated to ACTH-responsiveness of both COX2 and AKR1B7/B1. The pivotal role of AKR1B7 in ACTH-induced PGF2α release and functional coupling with COX2 was demonstrated using over- and down-expression in cell lines. PGF2α receptor was only detected in chromaffin cells, making medulla the primary target of PGF2α action. By comparing PGF2α-responsiveness of isolated cells and whole adrenal cultures, we demonstrated that PGF2α repressed glucocorticoid secretion by an indirect mechanism involving a decrease in catecholamine release which in turn decreased adrenal steroidogenesis. PGF2α may be regarded as a negative autocrine/paracrine regulator within a novel intra-adrenal feedback loop. The coordinated cell-specific regulation of COX2 and AKR1B7 ensures the generation of this stress-induced corticostatic signal