Magic™ Anti-CFH monoclonal antibody, clone N92700

The Maido high-altitude observatory located in Reunion Island (21 degrees S, 55.5 degrees E) is equipped with the Lidar1200, an innovative Raman lidar designed to measure the water vapor mixing ratio in the troposphere and the lower stratosphere, to perform long-term survey and processes studies in the vicinity of the tropopause. The calibration methodology is based on a GNSS (Global Navigation Satellite System) IWV (Integrated Water Vapor) dataset. The lidar water vapor measurements from November 2013 to October 2015 have been calibrated according to this methodology and used to evaluate the performance of the lidar. The 2-year operation shows that the calibration uncertainty using the GNSS technique is in good agreement with the calibration derived using radiosondes. During the MORGANE (Maido ObservatoRy Gaz and Aerosols NDACC Experiment) campaign (Reunion Island, May 2015), CFH (Cryogenic Frost point Hygrometer) radiosonde and Raman lidar profiles are compared and show good agreement up to 22 km asl; no significant biases are detected and mean differences are smaller than 9% up to 22 km asl.

Sialic acids (Sias) are the most abundant terminal sugar residues of glycoproteins and glycolipids on the surface of mammalian cells. The nervous tissue is the organ with the highest expression level of Sias. The 'sialylation' of glycoconjugates is performed via sialyltransferases, whereas 'desialylation' is done by sialidases or is a possible consequence of oxidative damage. Sialic acid residues on the neural cell surfaces inhibit complement and microglial activation, as well as phagocytosis of the underlying structures, via binding to (i) complement factor H (CFH) or (ii) sialic acid-binding immunoglobulin-like lectin (SIGLEC) receptors. In contrast, activated microglial cells show sialidase activity that desialylates both microglia and neurons, and further stimulates innate immunity via microglia and complement activation. The desialylation conveys neurons to become susceptible to phagocytosis, as well as triggers a microglial phagocytosis-associated oxidative burst and inflammation. Dysfunctions of the 'Sia-SIGLEC' and/or 'Sia-complement' axes often lead to neurological diseases. Thus, Sias on glycoconjugates of the intact glycocalyx and its desialylation are major regulators of neuroinflammation.