26 research outputs found
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Design and Performance of a Low Btu Fuel Rich-Quench-Lean Gas Turbine Combustor
General Electric Company is developing gas turbines and a high temperature desulfurization system for use in integrated gasification combined cycle (IGCC) power plants. High temperature desulfurization, or hot gas cleanup (HGCU), offers many advantages over conventional low temperature desulfurization processes, but does not reduce the relatively high concentrations of fuel bound nitrogen (FBN) that are typically found in low Btu fuel. When fuels containing bound nitrogen are burned in conventional gas turbine combustors, a significant portion of the FBN is converted to NO{sub x}. Methods of reducing the NO{sub x} emissions from IGCC power plants equipped with HGCU are needed. Rich-quench-lean (RQL) combustion can decrease the conversion of FBN to NO{sub x} because a large fraction of the FBN is converted into non-reactive N{sub 2} in a fuel rich stage. Additional air, required for complete combustion, is added in a quench stage. A lean stage provides sufficient residence time for complete combustion. Objectives General Electric has developed and tested a rich-quench-lean gas turbine combustor for use with low Btu fuels containing FBN. The objective of this work has been to design an RQL combustor that has a lower conversion of FBN to N{sub x} than a conventional low Btu combustor and is suitable for use in a GE heavy duty gas turbine. Such a combustor must be of appropriate size and scale, configuration (can-annular), and capable of reaching ``F`` class firing conditions (combustor exit temperature = 2550{degrees}F)
VEGF regulates local inhibitory complement proteins in the eye and kidney
10.1172/JCI86418Journal of Clinical Investigation1271199-21
VEGF regulates local inhibitory complement proteins in the eye and kidney
Outer retinal and renal glomerular functions rely on specialized vasculature maintained by VEGF that is produced by neighboring epithelial cells, the retinal pigment epithelium (RPE) and podocytes, respectively. Dysregulation of RPE- and podocyte-derived VEGF is associated with neovascularization in wet age-related macular degeneration (ARMD), choriocapillaris degeneration, and glomerular thrombotic microangiopathy (TMA). Since complement activation and genetic variants in inhibitory complement factor H (CFH) are also features of both ARMD and TMA, we hypothesized that VEGF and CFH interact. Here, we demonstrated that VEGF inhibition decreases local CFH and other complement regulators in the eye and kidney through reduced VEGFR2/PKC-α/CREB signaling. Patient podocytes and RPE cells carrying disease-associated CFH genetic variants had more alternative complement pathway deposits than controls. These deposits were increased by VEGF antagonism, a common wet ARMD treatment, suggesting that VEGF inhibition could reduce cellular complement regulatory capacity. VEGF antagonism also increased markers of endothelial cell activation, which was partially reduced by genetic complement inhibition. Together, these results suggest that VEGF protects the retinal and glomerular microvasculature, not only through VEGFR2-mediated vasculotrophism, but also through modulation of local complement proteins that could protect against complement-mediated damage. Though further study is warranted, these findings could be relevant for patients receiving VEGF antagonists