Anti-SACS (aa 100-200) polyclonal antibody

Single atom catalysts (SACs) with the maximized metal atom efficiency have sparked great attention. However, it is challenging to obtain SACs with high metal loading, high catalytic activity, and good stability. Herein, we demonstrate a new strategy to develop a highly active and stable Ag single atom in carbon nitride (Ag-N2C2/CN) catalyst with a unique coordination. The Ag atomic dispersion and Ag-N(2)C(2)configuration have been identified by aberration-correction high-angle-annular-dark-field scanning transmission electron microscopy (AC-HAADF-STEM) and extended X-ray absorption. Experiments and DFT calculations further verify that Ag-N(2)C(2)can reduce the H(2)evolution barrier, expand the light absorption range, and improve the charge transfer of CN. As a result, the Ag-N2C2/CN catalyst exhibits much better H(2)evolution activity than the N-coordinated Ag single atom in CN (Ag-N-4/CN), and is even superior to the Pt nanoparticle-loaded CN (Pt-NP/CN). This work provides a new idea for the design and synthesis of SACs with novel configurations and excellent catalytic activity and durability.

Bacterial infections in chicken eggs often cause mortality of embryos and clinical consequences in chicks but the pathological mechanism is unclear. We investigated the pathological changes and bacterial growth kinetics in dead and live embryos following infection with 2Escherichia colistrains with a different clinical background and with 1SalmonellaEnteritidis strain. In 2 experiments, 12-day-old embryos were infected via the allantoic sac with 100 mu l of 1 to 5 x 10(2)CFU/ml of one of the bacteria. In experiment 1, only dead embryos were sampled until 4 days postinfection (dpi), and surviving embryos were sampled at 5 dpi. In experiment 2, sampling was performed in dead and killed embryos sequentially at 1, 2, 3, and 4 dpi. The bacteria showed varying pathogenicity in embryos. The yolk sacs of dead embryos showed congestion, inflammation, damaged blood vessels, and abnormal endodermal epithelial cells. Such lesions were absent in the yolk sacs of negative control embryos and in those of embryos that survived infection. The livers and hearts of dead embryos showed congestion and lysed erythrocytes with no morphological changes in hepatocytes or myocardial cells. All bacteria multiplied rapidly in the yolks of infected embryos, although this did not predict survival. However, the livers of dead embryos contained significantly higher bacterial loads than the livers of the embryos that survived infection. The results provide evidence that lesions in the yolk sac, which have been neglected to date, coincide with embryonic mortality, underlining the importance of healthy yolk sacs for embryo survival.