Measuring Bremsstrahlung Photons in 200 GeV p+p Collisions

Direct photon production is an important observable in heavy ion collisions as photons are penetrating and therefore largely insensetive to final state effects that lead to jet quenching. Measurements of the fragmentation component to prompt photon yields in p+p and Au+Au collisions will provide both an important test of pQCD predictions and of predictions for modifications of this component in heavy ion collisions. By selecting photons associated with jets on the near side using hadron-photon correlations, fragmentation photons can be measured directly.Comment: 5 pages, 4 figures, poster presented at the 19th International Conference on Ultra-Relativistic Nucleus-Nucleus Collisions (QM2006

Measurements of Fragmentation Photons with the PHENIX Detector

Direct photons associated with jets provide a direct measurement of the effects of energy loss on the fragmentation of the parton as it propagates through the medium. Perturbative QCD calculations describe the direct photon cross section well at next-to-leading order, predicting a significant contribution from photons produced through parton fragmentation. Non-perturbative quantities such as the photon fragmentation function, which is poorly constrained, lead to large theoretical uncertainties. The measurement of photons correlated with jets in p+p collisions serves as an important test of these calculations and is an essential baseline measurement for comparison to A+A collisions. A natural way of selecting such photons is to study hadron-photon correlations. Results for the production of photons associated with high pT hadron triggers are presented for PHENIX p+p data at 200 GeV center-of-mass energy.Comment: 4 pages, 4 figures - To appear in the conference proceedings for Quark Matter 2009, March 30 - April 4, Knoxville, Tennessee Corrected typos, changed conten

Addressing racial inequalities in dental education: decolonising the dental curricula

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Cranial nerve outcomes in regionally recurrent head & neck melanoma after sentinel lymph node biopsy

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/156007/1/lary28243.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/156007/2/lary28243_am.pd

Chromosomal instability by mutations in the novel minor spliceosome component CENATAC

Aneuploidy is the leading cause of miscarriage and congenital birth defects, and a hallmark of cancer. Despite this strong association with human disease, the genetic causes of aneuploidy remain largely unknown. Through exome sequencing of patients with constitutional mosaic aneuploidy, we identified biallelic truncating mutations in CENATAC (CCDC84). We show that CENATAC is a novel component of the minor (U12-dependent) spliceosome that promotes splicing of a specific, rare minor intron subtype. This subtype is characterized by AT-AN splice sites and relatively high basal levels of intron retention. CENATAC depletion or expression of disease mutants resulted in excessive retention of AT-AN minor introns in similar to 100 genes enriched for nucleocytoplasmic transport and cell cycle regulators, and caused chromosome segregation errors. Our findings reveal selectivity in minor intron splicing and suggest a link between minor spliceosome defects and constitutional aneuploidy in humans.Peer reviewe

Cofactor-mediated conformational control in the bifunctional kinase/RNase Ire1

<p>Abstract</p> <p>Background</p> <p>Ire1 is a signal transduction protein in the endoplasmic reticulum (ER) membrane that serves to adjust the protein-folding capacity of the ER according to the needs of the cell. Ire1 signals, in a transcriptional program, the unfolded protein response (UPR) via the coordinated action of its protein kinase and RNase domains. In this study, we investigated how the binding of cofactors to the kinase domain of Ire1 modulates its RNase activity.</p> <p>Results</p> <p>Our results suggest that the kinase domain of Ire1 initially binds cofactors without activation of the RNase domain. RNase is activated upon a subsequent conformational rearrangement of Ire1 governed by the chemical properties of bound cofactors. The conformational step can be selectively inhibited by chemical perturbations of cofactors. Substitution of a single oxygen atom in the terminal β-phosphate group of a potent cofactor ADP by sulfur results in ADPβS, a cofactor that binds to Ire1 as well as to ADP but does not activate RNase. RNase activity can be rescued by thiophilic metal ions such as Mn²⁺and Cd²⁺, revealing a functional metal ion-phosphate interaction which controls the conformation and RNase activity of the Ire1 ADP complex. Mutagenesis of the kinase domain suggests that this rearrangement involves movement of the αC-helix, which is generally conserved among protein kinases. Using X-ray crystallography, we show that oligomerization of Ire1 is sufficient for placing the αC-helix in the active, cofactor-bound-like conformation, even in the absence of cofactors.</p> <p>Conclusions</p> <p>Our structural and biochemical evidence converges on a model that the cofactor-induced conformational change in Ire1 is coupled to oligomerization of the receptor, which, in turn, activates RNase. The data reveal that cofactor-Ire1 interactions occur in two independent steps: binding of a cofactor to Ire1 and subsequent rearrangement of Ire1 resulting in its self-association. The pronounced allosteric effect of cofactors on protein-protein interactions involving Ire1's kinase domain suggests that protein kinases and pseudokinases encoded in metazoan genomes may use ATP pocket-binding ligands similarly to exert signaling roles other than phosphoryl transfer.</p

Glycosylation status of the C. albicans cell wall affects the efficiency of neutrophil phagocytosis and killing but not cytokine signaling

The cell wall of the opportunistic human fungal pathogen, Candida albicans is a complex, layered network of rigid structural polysaccharides composed of β-glucans and chitin that is covered with a fibrillar matrix of highly glycosylated mannoproteins. Poly-morphonuclear cells (PMNs, neutrophils) are the most prevalent circulating phagocytic leukocyte in peripheral blood and they are pivotal in the clearance of invading fungal cells from tissues. The importance of cell-wall mannans for the recognition and uptake of C. albicans by human PMNs was therefore investigated. N- and O-glycosylation-deficient mutants were attenuated in binding and phagocytosis by PMNs and this was associated with reduced killing of C. albicans yeast cells. No differences were found in the production of the respiratory burst enzyme myeloperoxidase (MPO) and the neutrophil chemokine IL-8 in PMNs exposed to control and glycosylation-deficient C. albicans strains. Thus, the significant decrease in killing of glycan-deficient C. albicans strains by PMNs is a consequence of a marked reduction in phagocytosis rather than changes in the release of inflammatory mediators by PMNs

Polymeric drift control adjuvants for agricultural spraying

The movement of a pesticide or herbicide to an off-target site during agricultural spraying can cause injury to wildlife, plants and contamination of surface water. This phenomenon is known as spray drift and can be controlled by spraying during favorable environmental conditions, and by using low drift nozzles and drift control adjuvants (DCAs). Polymeric DCAs are the most common type of DCA and function by increasing the droplet size produced during spraying. There are, however, two main drawbacks of polymeric DCAs; they are prone to mechanical degradation during spraying which reduces their performance and they can produce oversized drops which reduces the efficacy of the spray. In this trend article, existing DCA technology is reviewed including the mechanism through which they function. This then provides a platform for the discussion of novel polymeric architectures which have currently not been applied in DCA formulations