No abstract

Nitrogen oxides (NO x ) play a key role in regulating the oxidizing capacity of the atmosphere through controlling the abundance of O3, OH, and other important gas and particle species. Some recent studies have suggested that particulate nitrate, which is conventionally considered as the ultimate oxidation product of NO x , can undergo “renoxification” via photolysis, recycling NO x and HONO back to the gas phase. However, there are large discrepancies in estimates of the importance of this channel, with reported renoxification rate constants spanning three orders of magnitude. In addition, previous laboratory studies derived the rate constant using bulk particle samples collected on substrates instead of suspended particles. In this work, we study renoxification of suspended submicron particulate sodium and ammonium nitrate through controlled laboratory photolysis experiments using an environmental chamber. We find that, under atmospherically relevant wavelengths and relative humidities, particulate inorganic nitrate releases NO x and HONO less than 10 times as rapidly as gaseous nitric acid, putting our measurements on the low end of recently reported renoxification rate constants. To the extent that our laboratory conditions are representative of the real atmosphere, renoxification from the photolysis of inorganic particulate nitrate appears to play a limited role in contributing to the NO x and OH budgets in remote environments. These results are based on simplified model systems; future studies should investigate renoxification of more complex aerosol mixtures that represent a broader spectrum of aerosol properties to better constrain the photolysis of ambient aerosols.

Background Lymphatics are important for their conduit functions of transporting antigen, immune cells, and inflammatory mediators to draining lymph nodes and to the general circulation. Lymphangiogenesis is involved in many pathologic processes; however, the roles for lymphatic responses in transplantation have not been thoroughly investigated. Methods Mice were made diabetic by a single high dose of streptozotocin and then received islet allografts. Animals were treated with three different lymphatic inhibitors. FTY720, an analog of sphingosine 1-phosphate, inhibited lymphocyte migration into afferent and efferent lymphatics. Sunitinib, a kinase inhibitor, blocked several receptors, including vascular endothelial growth factor receptor 3 (VEGFR3), the major growth factor receptor for lymphatic endothelial cells. Anti-VEGFR3 monoclonal antibody specifically inhibited VEGFR3. Diabetes was determined by daily monitoring of blood glucose levels. Inflammation within islet grafts was assessed by immunohistochemistry for insulin, T cells (CD3), and lymphatics (LYVE-1). Results After transplantation, lymphangiogenesis occurred in islet allografts and in draining lymph nodes. FTY720, sunitinib, and anti-VEGFR3 each inhibited lymphangiogenesis in the islets and significantly prolonged allograft survival. Immunofluorescent staining demonstrated that administration of each of the lymphatic inhibitors resulted in preservation of islets and β-cells along with a markedly reduced infiltration of T cells into the grafts. Conclusion Lymphangiogenesis occurs in islet allografts in response to inflammation and plays a key role in the islet inflammation in alloimmunity. Interfering with lymphatic function leads to inhibition of lymphangiogenesis and prolonged or indefinite allograft survival. These observations suggest new therapeutic targets for rejection and tolerance.

Isoflurane-mediated enhancement of GABA-triggered [Ca2+]i release results from membrane depolarization with subsequent activation of VDCCs and further Ca2+-induced Ca2+ release from the ryanodine-sensitizing Ca2+ store. An increase in [Ca2+]i, caused by activation of the GABAA receptor and opening of VDCCs, is necessary for isoflurane-induced calcium overload of immature rat hippocampal neurons, which may be involved in the mechanism of an isoflurane-induced neurotoxic effect in the developing rodent brain.