18 research outputs found

    The Proton Spin and the Wigner Rotation

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    It is shown that in both the gluonic and strange sea explanations of the Ellis-Jaffe sum rule violation discovered by the European Muon Collaboration (EMC), the spin of the proton, when viewed in in its rest reference frame, could by fully provided by quarks and antiquarks within a simple quark model picture, taken into account the relativistic effect from the Wigner rotation.Comment: 13 latex page

    Epigenetics and the estrogen receptor

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    The position effect variegation in Drosophila and Schizosaccharomyces pombe, and higher-order chromatin structure regulation in yeast, is orchestrated by modifier genes of the Su(var) group, (e.g., histone deacetylases ([HDACs]), protein phosphatases) and enhancer E(Var) group (e.g., ATP [adenosine 5\u27-triphosphate]-dependent nucleosome remodeling proteins). Higher-order chromatin structure is regulated in part by covalent modification of the N-terminal histone tails of chromatin, and histone tails in turn serve as platforms for recruitment of signaling modules that include nonhistone proteins such as heterochromatin protein (HP1) and NuRD. Because the enzymes governing chromatin structure through covalent modifications of histones (acetylation, methylation, phosphorylation, ubiquitination) can also target nonhistone substrates, a mechanism is in place by which epigenetic regulatory processes can affect the function of these alternate substrates. The posttranslational modification of histones, through phosphorylation and acetylation at specific residues, alters chromatin structure in an orchestrated manner in response to specific signals and is considered the basis of a histone code. In an analogous manner, specific residues within transcription factors form a signaling module within the transcription factor to determine genetic target specificity and cellular fate. The architecture of these signaling cascades in transcription factors (SCITs) are poorly understood. The regulation of estrogen receptor (ERalpha) by enzymes that convey epigenetic signals is carefully orchestrated and is reviewed here

    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

    Pulmonary Lobe Segmentation in CT Examinations Using Implicit Surface Fitting

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    Robotic traverse and sample return strategies for a lunar farside mission to the Schrodinger basin

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    Most of the highest priority objectives for lunar science and exploration (e.g., NRC, 2007) require sample return. Studies of the best places to conduct that work have identified Schrödinger basin as a geologically rich area, able to address a significant number of these scientific concepts. In this study traverses were designed for a robotic mission within previously identified crewed landing sites in Schrödinger basin. Traverse routes and sampling locations were identified using LROC imagery and LOLA topography data, combined with a theoretical rover travel and operations model. The findings of this investigation highlight the need to consider increased rover capabilities. A significant number of samples that can address many of the NRC (2007) scientific goals can be returned in a robotic mission during one period of lunar illumination (~14 Earth days) using specifications from previous lunar rovers
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