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Bromine radicals (Br + BrO) are important atmospheric species owing to their ability to catalytically destroy ozone as well as their potential impacts on the oxidative pathways of many trace gases, including dimethylsulfide and mercury. Using space‐based observations of BrO, recent studies have reported rapid enhancements of tropospheric BrO over large areas (so called “BrO explosions”) connected to near‐surface ozone depletion occurring in polar spring. However, the source(s) of reactive bromine and mechanism(s) that initiate these BrO explosions are uncertain. In this study, we investigate the relationships between Arctic BrO explosions and two of the proposed sources of reactive bromine: sea‐salt aerosol (SSA) generated from blowing snow and first‐year (seasonal) sea ice. We use tropospheric column BrO derived from the Ozone Monitoring Instrument (OMI) in conjunction with the Goddard Earth Observing System Version 5 (GEOS‐5) data assimilation system provided by National Aeronautics and Space Administration Global Modeling and Assimilation Office. Case studies demonstrate a strong association between the temporal and spatial extent of OMI‐observed BrO explosions and the GEOS‐5 simulated blowing snow‐generated SSA during Arctic spring. Furthermore, the frequency of BrO explosion events observed over the 11‐year record of OMI exhibits significant correlation with a time series of the simulated SSA emission flux in the Arctic and little to no correlation with a time series of satellite‐based first‐year sea ice area. Therefore, we conclude that SSA generated by blowing snow is an important factor in the formation of the BrO explosion observed from space during Arctic spring. OMI‐observed Arctic tropospheric BrO explosions are associated with GEOS‐5 simulated sea‐salt aerosols (SSAs) from wind‐driven blowing snowThe 11‐year time series analysis shows that the Arctic BrO explosion frequency and simulated blowing snow SSA emission flux are correlatedThe satellite‐based record of first‐year sea ice area does not show significant correlation with the Arctic BrO explosion frequency

Engagement of beta1 integrins in terminally differentiated human B cell lines, such as ARH-77, leads to prominent tyrosine phosphorylation of the p130 Crk-associated substrate (Cas). Cas regulates the assembly of several SH2 and SH3 domain-containing proteins into signaling complexes, which are potentially involved in the propagation of downstream signals. We demonstrate here that immunoprecipitated Cas from beta1 integrin-stimulated ARH-77 cells was associated with tyrosine kinase and phosphatase activities and that integrin ligation led to the recruitment of at least p59(Fyn) tyrosine kinase and SHP2 tyrosine phosphatase in Cas immune complexes. Cotransfection studies in COS-7 cells further indicated that Fyn/Cas physical interaction and Fyn-mediated Cas phosphorylation required amino acids 638-889 in the C-terminal region of Cas. This sequence contains both c-Src SH2 and SH3 domain-binding motifs. In vitro binding studies using glutathione S-transferase fusion proteins derived from the SH2 or SH3 domains of Fyn suggested that both Fyn domains can participate in Fyn/Cas interaction. These data implicate Fyn and SHP2 as potential modulators of Cas signaling complexes in B cells.

Integrin ligation initiates intracellular signaling events, among which are the activation of protein tyrosine kinases. The related adhesion focal tyrosine kinase (RAFTK), also known as PYK2 and CAKbeta, is a tyrosine kinase that is homologous to the focal adhesion kinase (FAK) p125FAK. The structure of RAFTK is similar to p125FAK in that it lacks a transmembrane region, does not contain Src homology 2 or 3 domains, and has a proline-rich region in its C terminus. Here we report that RAFTK is a target for beta1-integrin-mediated tyrosine phosphorylation in both transformed and normal human B cells. Ligation of the B cell antigen receptor also induced tyrosine phosphorylation of RAFTK. Phosphorylation of RAFTK following integrin- or B cell antigen receptor-mediated stimulation was decreased by prior treatment of cells with cytochalasin B, indicating that this process was at least partially cytoskeleton-dependent. One of the tyrosine-phosphorylated substrates after integrin stimulation in fibroblasts is p130cas, which can associate with p125FAK. RAFTK also interacted constitutively with p130cas in B cells, since p130cas was detected in RAFTK immunoprecipitates. Although the function of RAFTK remains unknown, these data suggest that RAFTK may have a significant function in integrin-mediated signaling pathways in B cells.

The Crk-associated substrate p130(Cas) (Cas) and the recently described human enhancer of filamentation 1 (HEF1) are two proteins with similar structure (64% amino acid homology), which are thought to act as "docking" molecules in intracellular signaling cascades. Both proteins contain an N-terminal Src homology (SH), three domain and a cluster of SH2 binding motifs. Here we show that ligation of either beta1 integrin or B cell antigen receptor (BCR) on human tonsillar B cells and B cell lines promoted tyrosine phosphorylation of HEF1. In contrast, Cas tyrosine phosphorylation was observed in certain B cell lines but not in tonsillar B cells, indicating a more general role for HEF1 in B cell signaling. Interestingly, pretreatment of tonsillar B cells with cytochalasin B dramatically reduced both integrin- and BCR-induced HEF1 phosphorylation, suggesting that some component of the BCR-mediated signaling pathway is closely linked with a cytoskeletal reorganization. Both HEF1 and Cas were found to complex with the related adhesion focal tyrosine kinase (RAFTK), and when tyrosine phosphorylated, with the adapter molecule CrkL. In addition, the two molecules were detected in p53/56(Lyn) immunoprecipitates, and Lyn kinase was found to specifically bind the C-terminal proline-rich sequence of Cas in an in vitro binding assay. These associations implicate HEF1 and Cas as important components in a cytoskeleton-linked signaling pathway initiated by ligation of beta1 integrin or BCR on human B cells.

A CELLULAR immune response to antigenic stimulation is frequently accompanied by a humoral immune response. This conjugal behaviour has complicated an understanding of the specific steps of a cellular immune response. Humoral immunity is easily measured apart from cellular immunity. Specific measurement of cellular immunity however, is complicated by the ability of some cells in lymphoid organs to produce both complement1and antibody2. Brunner et al.3have introduced a 51Cr release technique for measuring cellular immunity, and our modifications4have increased the sensitivity of the procedure and the certainty that cellular immunity is being detected. We have now used this method to detect the in vitro induction of cellular immunity.

The photochemistry of the hydroxyl radical (OH) in the middle atmosphere involves the action of solar ultraviolet radiation in many respects. The production of stratospheric OH is initiated through the photodissociation of ozone, and in the mesosphere, OH is produced directly from the photolysis of water vapor. We present an analysis of measurements of the vertical column abundance of OH from Fritz Peak Observatory, Colorado, for seasonal and solar cycle variability. The OH column data span over two 11‐year solar cycles and include a wide range of diurnal and seasonal conditions. Hydroxyl abundances show distinct annual and semiannual cycles, with amplitudes of 4.4% and 2.5%, respectively. About half of the seasonal variation in OH can be explained by the annual cycle of ultraviolet intensity, and by annual and semiannual cycles in ozone and water vapor in the middle atmosphere. On longer time scales, a positive correlation with the NOAA MgII solar index is observed. The amplitude of 11‐year solar cycle variations in OH is 4.2 ± 2.4%, which is consistent with photochemical model calculations that consider changes in ozone and water vapor photodissociation rates. Changes in the vertical distribution of ozone over the solar cycle are found to have a smaller effect on the OH column.