Spin dependence in high pT2p^{2}_{T} elastic pp and np scattering

Using the polarized proton capability of the Argonne ZGS the authors recently made 90 degrees /sub cm/ measurements of elastic pp scattering from 6 to 11.75 GeV/c, determining the parallel and anti- parallel pure initial spin state cross sections and the associated spin-spin parameter A/sub nn/ with the spins normal to the scattering plane. They find that the parallel to anti-parallel cross section ratio rises dramatically from 1.2+or-.06 at p/sub t//sup 2/=3.3 (GeV /c)/sup 2/ to 3.2+or-.4 at 4.8 (GeV/c)/sup 2/, similar to the p/sub T //sup 2/ dependence previously observed at the fixed laboratory momentum of 11.75 GeV/c. They have also extended the measurements at 6 GeV/c and find that A/sub nn/ has a small but sharp rise at 90 degrees /sub cm/. In addition a month of 12 GeV/c polarized deuteron acceleration in the ZGS enabled them to measure two A/sub nn/ at two points at 6 GeV/c for np elastic scattering: A/sub nn/=-.17+or-.04 at p/sub T//sup 2/=.8, A/sub nn/=-.19+or-.05 at P/sub T//sup 2/=1.0. These values are opposite in sign from the pp results at the same momentum. (4 refs)

Aberrant Expression of Cell Cycle Regulator 14-3-3-σ and E-Cadherin in a Metastatic Cholangiocarcinoma in a Vervet Monkey (Chlorocebus pygerythrus).

We present a unique case of metastatic cholangiocarcinoma with concurrent abdominal cestodiasis in an African green monkey (Chlorocebus pygerythrus) that presented with respiratory insufficiency and abdominal discomfort. There were multiple white-grey masses in the liver and colonic serosa alongside intra-abdominal parasitic cysts. Histopathologically, the liver masses were composed of poorly-differentiated epithelial cells that formed densely cellular solid areas and trabeculae. The neoplastic cells were strongly immunopositive for CK7 but negative for Hep-Par1 antigen, which confirmed a diagnosis of cholangiocarcinoma. Interestingly, there was strong and diffuse neoexpression in the tumour of the cell cycle regulator 14-3-3σ, which is not constitutively expressed in normal liver. There was aberrantly strong expression of E-cadherin, a key cell-cell adhesion protein, in neoplastic cells with evidence of cytoplasmic internalization. This is the first immunohistochemical analysis of 14-3-3σ and E-cadherin in a liver neoplasm in an animal species and the use of these markers requires further investigation in animal liver neoplasms. [Abstract copyright: Copyright © 2020 Elsevier Ltd. All rights reserved.

Lung adenocarcinoma promotion by air pollutants

A complete understanding of how exposure to environmental substances promotes cancer formation is lacking. More than 70 years ago, tumorigenesis was proposed to occur in a two-step process: an initiating step that induces mutations in healthy cells, followed by a promoter step that triggers cancer development1. Here we propose that environmental particulate matter measuring ≤2.5 μm (PM2.5), known to be associated with lung cancer risk, promotes lung cancer by acting on cells that harbour pre-existing oncogenic mutations in healthy lung tissue. Focusing on EGFR-driven lung cancer, which is more common in never-smokers or light smokers, we found a significant association between PM2.5 levels and the incidence of lung cancer for 32,957 EGFR-driven lung cancer cases in four within-country cohorts. Functional mouse models revealed that air pollutants cause an influx of macrophages into the lung and release of interleukin-1β. This process results in a progenitor-like cell state within EGFR mutant lung alveolar type II epithelial cells that fuels tumorigenesis. Ultradeep mutational profiling of histologically normal lung tissue from 295 individuals across 3 clinical cohorts revealed oncogenic EGFR and KRAS driver mutations in 18% and 53% of healthy tissue samples, respectively. These findings collectively support a tumour-promoting role for PM2.5 air pollutants and provide impetus for public health policy initiatives to address air pollution to reduce disease burden

Vacuum chamber thermal protection for the APS (Advanced Photon Source)

The addition of undulators and wigglers into synchrotron storage rings created new problems in terms of protecting the integrity of the ring vacuum chamber. If the photon beam from these devices were missteered into striking an inadequately cooled section of the storage ring vacuum chamber, the structural strength might be reduced sufficiently that the vacuum envelope could be penetrated, resulting in long downtime of the storage ring. The new generation of high-energy synchrotron light sources will produce photon beams of such high power density that cooling of the vacuum chamber will not prevent a potential penetration of the vacuum envelope, and other methods of preventing this occurrence will be required. Since active methods will be used to ensure that the beams are delivered to beam lines for users during normal operation, there is a need for passive protection methods during non-routine operation, such as turning on new beam lines, injection, etc., when the active systems may be disabled. In addition, the passive methods could prevent the problem from arising and provide the rapid time response necessary for the highest power beams, a property that might not be easily and reliably provided by active methods during the early operation of these machines. This paper summarizes the results of a task group that studied the problem and outlines passive methods of protection for the Advanced Photon Source (APS). 2 refs., 3 figs., 1 tab

Converging evidence does not support GIT1 as an ADHD risk gene

Attention-Deficit/Hyperactivity Disorder (ADHD) is a common neuropsychiatric disorder with a complex genetic background. The G protein-coupled receptor kinase interacting ArfGAP 1 (GIT1) gene was previously associated with ADHD. We aimed at replicating the association of GIT1 with ADHD and investigated its role in cognitive and brain phenotypes. Gene-wide and single variant association analyses for GIT1 were performed for three cohorts: (1) the ADHD meta-analysis data set of the Psychiatric Genomics Consortium (PGC, N=19,210), (2) the Dutch cohort of the International Multicentre persistent ADHD CollaboraTion (IMpACT-NL, N=225), and (3) the Brain Imaging Genetics cohort (BIG, N=1,300). Furthermore, functionality of the rs550818 variant as an expression quantitative trait locus (eQTL) for GIT1 was assessed in human blood samples. By using Drosophila melanogaster as a biological model system, we manipulated Git expression according to the outcome of the expression result and studied the effect of Git knockdown on neuronal morphology and locomotor activity. Association of rs550818 with ADHD was not confirmed, nor did a combination of variants in GIT1 show association with ADHD or any related measures in either of the investigated cohorts. However, the rs550818 risk-genotype did reduce GIT1 expression level. Git knockdown in Drosophila caused abnormal synapse and dendrite morphology, but did not affect locomotor activity. In summary, we could not confirm GIT1 as an ADHD candidate gene, while rs550818 was found to be an eQTL for GIT1. Despite GIT1's regulation of neuronal morphology, alterations in gene expression do not appear to have ADHD-related behavioral consequences

Genomics of quality traits

The quality attributes of cereal grains are valued in the context of a complex food chain that integrates outputs achievable by breeding, production, and processing. New processing technologies, environmental change, and changes in consumer preferences demand that quality attributes of wheat and barley need to be continually modified. The advances in the genomics of quality described in this chapter provide the basis for ensuring that the genetic approaches encompassing the complexities of the gene networks underpinning quality attributes can meet the challenges presented by the rapid changes occurring within the food chain

Brain charts for the human lifespan

10.1038/s41586-022-04554-yNature6047906525-53