Distribution of Hydrocarbons and Microbial Populations Related to Sedimentation Processes in Lower Cook Inlet and Norton Sound, Alaska

In spring and summer 1978 and spring 1979 an integrated study was carried out to examine the interrelationships of physical (sediment deposition), chemical (organic carbon and hydrocarbon concentrations), and biological (microbial populations and activities) factors in the Cook Inlet and Norton Sound regions with respect to the probable sinks and fates of hydrocarbon contaminants within these ecosystems. Most of the fine-grained sediment entering Cook Inlet is transported out of the inlet into Shelikof Strait. However, significant sediment accumulation occurs within areas of Kamishak and Kachemak bays. In Norton Sound, sediment from the Yukon River is transported counterclockwise around the embayment and approximately 50% is deposited in the nearshore regions of the sound. In both regions, areas of high sediment accumulation are richer in organic carbon and hydrocarbon derived from land than are areas of low sediment accumulation. In general, areas with high sediment accumulation rates for fine-grained particles are also areas of relatively high microbial activity. Results suggest that these elevated microbial activities reflect biodegradation of detrital carbon associated with these particles. Also, the Cook Inlet and Norton Sound region were found to be free from petroleum hydrocarbon contamination (with the exception of one area in Cook Inlet). No evidence was found of hydrocarbon accumulation resulting from a gas seepage in Norton Sound, nor for accumulation of hydrocarbons in sediments of lower Cook Inlet and Shelikof Strait from oil well operations in upper Cook Inlet.Key words: arctic marine ecosystems, sedimentation, microorganism, hydrocarbons, lower Cook Inlet, Norton SoundMots clés: écosystèmes marins arctiques, sédimentation, micro-organismes, hydrocarbons, sud de l'inlet Cook, bras de mer Norto

CD11b activation suppresses TLR-dependent inflammation and autoimmunity in systemic lupus erythematosus

Genetic variations in the ITGAM gene (encoding CD11b) strongly associate with risk for systemic lupus erythematosus (SLE). Here we have shown that 3 nonsynonymous ITGAM variants that produce defective CD11b associate with elevated levels of type I interferon (IFN-I) in lupus, suggesting a direct link between reduced CD11b activity and the chronically increased inflammatory status in patients. Treatment with the small-molecule CD11b agonist LA1 led to partial integrin activation, reduced IFN-I responses in WT but not CD11b-deficient mice, and protected lupus-prone MRL/ Lpr mice from end-organ injury. CD11b activation reduced TLR-dependent proinflammatory signaling in leukocytes and suppressed IFN-I signaling via an AKT/FOXO3/IFN regulatory factor 3/7 pathway. TLR-stimulated macrophages from CD11B SNP carriers showed increased basal expression of IFN regulatory factor 7 (IRF7) and IFN-β, as well as increased nuclear exclusion of FOXO3, which was suppressed by LA1-dependent activation of CD11b. This suggests that pharmacologic activation of CD11b could be a potential mechanism for developing SLE therapeutics