Measurement of the Photon Structure Function F2gamma with the L3 Detector at LEP

The e+e- -> e+e- hadrons reaction, where one of the two electrons is detected in a low polar-angle calorimeter, is analysed in order to measure the hadronic photon structure function F2gamma . The full high-energy and high-luminosity data set, collected with the L3 detector at centre-of-mass energies 189-209GeV, corresponding to an integrated luminosity of 608/pb is used. The Q^2 range 11-34GeV^2 and the x range 0.006-0.556 are considered. The data are compared with recent parton density functions

The evolving SARS-CoV-2 epidemic in Africa: Insights from rapidly expanding genomic surveillance

INTRODUCTION Investment in Africa over the past year with regard to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) sequencing has led to a massive increase in the number of sequences, which, to date, exceeds 100,000 sequences generated to track the pandemic on the continent. These sequences have profoundly affected how public health officials in Africa have navigated the COVID-19 pandemic. RATIONALE We demonstrate how the first 100,000 SARS-CoV-2 sequences from Africa have helped monitor the epidemic on the continent, how genomic surveillance expanded over the course of the pandemic, and how we adapted our sequencing methods to deal with an evolving virus. Finally, we also examine how viral lineages have spread across the continent in a phylogeographic framework to gain insights into the underlying temporal and spatial transmission dynamics for several variants of concern (VOCs). RESULTS Our results indicate that the number of countries in Africa that can sequence the virus within their own borders is growing and that this is coupled with a shorter turnaround time from the time of sampling to sequence submission. Ongoing evolution necessitated the continual updating of primer sets, and, as a result, eight primer sets were designed in tandem with viral evolution and used to ensure effective sequencing of the virus. The pandemic unfolded through multiple waves of infection that were each driven by distinct genetic lineages, with B.1-like ancestral strains associated with the first pandemic wave of infections in 2020. Successive waves on the continent were fueled by different VOCs, with Alpha and Beta cocirculating in distinct spatial patterns during the second wave and Delta and Omicron affecting the whole continent during the third and fourth waves, respectively. Phylogeographic reconstruction points toward distinct differences in viral importation and exportation patterns associated with the Alpha, Beta, Delta, and Omicron variants and subvariants, when considering both Africa versus the rest of the world and viral dissemination within the continent. Our epidemiological and phylogenetic inferences therefore underscore the heterogeneous nature of the pandemic on the continent and highlight key insights and challenges, for instance, recognizing the limitations of low testing proportions. We also highlight the early warning capacity that genomic surveillance in Africa has had for the rest of the world with the detection of new lineages and variants, the most recent being the characterization of various Omicron subvariants. CONCLUSION Sustained investment for diagnostics and genomic surveillance in Africa is needed as the virus continues to evolve. This is important not only to help combat SARS-CoV-2 on the continent but also because it can be used as a platform to help address the many emerging and reemerging infectious disease threats in Africa. In particular, capacity building for local sequencing within countries or within the continent should be prioritized because this is generally associated with shorter turnaround times, providing the most benefit to local public health authorities tasked with pandemic response and mitigation and allowing for the fastest reaction to localized outbreaks. These investments are crucial for pandemic preparedness and response and will serve the health of the continent well into the 21st century

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

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

Characterization of Pseudomonas putida genes responsive to nutrient limitation

Microbiology15061661-1669MROB

Manufacture of 8.4 m segments for the GMT primary mirror

The Richard F. Caris Mirror Lab at the University of Arizona continues production of 8.4 m lightweight honeycomb segments for the primary mirror of the Giant Magellan Telescope. GMT will have a center segment surrounded by six off-Axis segments, plus an additional off-Axis segment to allow continuous operation as segments are removed for coating. The second off-Axis segment was completed and accepted in 2019. We are currently polishing the optical surface of off-Axis Segment 3. We have completed work on the rear surfaces of Segment 4, the center segment, and offaxis Segment 5. We are assembling the mold for off-Axis Segment 6 with the spin-casting scheduled for March 2021. © 2020 SPIE.Immediate accessThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Production of 8.4 m primary mirror segments for GMT

The Richard F. Caris Mirror Lab at the University of Arizona continues production of 8.4 m lightweight honeycomb segments for the primary mirror of the Giant Magellan Telescope. GMT's 25 m primary mirror consists of a center segment surrounded by six off-axis segments, with an additional off-axis segment to allow continuous operation as segments are removed for coating. We cast the sixth segment (5 off-axis segments + center segment) in March 2021. As of June 2022 we have tentatively completed polishing of the third off-axis segment, and we are in the process of grinding the optical surface of off-axis Segment 5. For Segment 3, we improved the measurement accuracy for small-scale structure near the edge of the mirror, which has been a challenge for the off-axis segments. In addition to full-aperture interferometry and deflectometry, we used a 20 cm test plate to obtain high-resolution interferometric measurements of the edge. © COPYRIGHT SPIE. Downloading of the abstract is permitted for personal use only.Immediate accessThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]