Atmospheric Channel Characteristics for Quantum Communication with Continuous Polarization Variables

We investigate the properties of an atmospheric channel for free space quantum communication with continuous polarization variables. In our prepare-and-measure setup, coherent polarization states are transmitted through an atmospheric quantum channel of 100m length on the roof of our institute's building. The signal states are measured by homodyne detection with the help of a local oscillator (LO) which propagates in the same spatial mode as the signal, orthogonally polarized to it. Thus the interference of signal and LO is excellent and atmospheric fluctuations are autocompensated. The LO also acts as spatial and spectral filter, which allows for unrestrained daylight operation. Important characteristics for our system are atmospheric channel influences that could cause polarization, intensity and position excess noise. Therefore we study these influences in detail. Our results indicate that the channel is suitable for our quantum communication system in most weather conditions.Comment: 6 pages, 4 figures, submitted to Applied Physics B following an invitation for the special issue "Selected Papers Presented at the 2009 Spring Meeting of the Quantum Optics and Photonics Section of the German Physical Society

Proliferation, apoptosis and their regulatory protein expression in colorectal adenomas and serrated lesions

Background Adenomas and serrated lesions represent heterogeneous sets of early precursors in the colorectum with varying malignant potential. They are often distinguished by their histopathologic differences, but little is known about potential differences in regulation of epithelial proliferation and apoptosis. Methods We conducted a protein expression analysis using tissue microarrays of 625 colorectal adenomas and 142 serrated lesions to determine potential differences in regulation of epithelial proliferation and apoptosis. We quantitated proliferation with Ki-67; apoptosis with activated caspase-3 (CASP3); up- and down-regulators of proliferation with cyclin D1, p16INK2, and p21Cip1; and apoptosis regulators with BAX, BCL2, and survivin. Linear mixed effects models and circos diagrams were used to determine relationships among expression and lesion characteristics. Results Adenomas had a significantly higher CASP-3 labeling index (LI) than serrated lesions, resulting in a lower net growth ratio (Ki-67 LI/activated CASP-3 LI, p-value<0.0001). Cyclin D1 LI, p16 LI and p21 LI were lower in adenomas compared to serrated lesions, while expression of both BCL2 and BAX were higher (p <0.001). Among adenomas, cyclin D1 LI and p16 LI levels increased with greater villous component, and the highest BAX expression was detected in adenomas larger than 2 cm (both p<0.0001). Right-sided adenomas had higher CASP3 LI than left colorectal adenomas (p = 0.008). Significant differences in cyclin D1 LI, p21 LI and survivin LI were also observed across histopathologic subtypes of serrated lesions. Conclusions Our findings demonstrate different patterns of regulatory protein expression in adenomas than serrated lesions, especially involving apoptosis

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

SPAT 15 - Assessment

In the Spring of 1997, the Department of Energy's Department Standards Committee (DSC) convened a Standards Process Action Team (SPAT-15) to evaluate assessment processes within the DOE complex. If time and resources permitted, the team was also to evaluate assessment processes used by private industry conducting similar work and activities. The specific task statement was as follows: "Define the attributes of assessment programs that effectively support organizational feedback and improvement of safety systems at all the different levels of contractor and Department organizations." The team gathered information on existing assessment programs through surveys and presentations by representatives from national laboratories, processing facilities, and remediation sites. Examples of assessment programs described in this report encompass site-wide, individual facility, and task level applications within the DOE compIe