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961.
Evidence for syntrophic butyrate metabolism under sulfate-reducing conditions in a hydrocarbon-contaminated aquifer 总被引:1,自引:0,他引:1
The importance of syntrophy in the degradation of butyrate in an aquifer where sulfate reduction was shown to be an important terminal electron-accepting process was assessed. Hydrocarbon-contaminated aquifer sediments coupled butyrate degradation to sulfate reduction and methane production. Butyrate degradation in methanogenic microcosms was inhibited by the addition of 2-bromoethanesulfonic acid, and was restored by the addition of 10 mM sulfate and a hydrogen- and formate-using sulfate reducer, but not by the addition of 10 mM sulfate alone. Molybdate addition inhibited butyrate degradation in sulfate-reducing microcosms. The addition of CO, which inhibits hydrogenases, to sulfate-reducing microcosms inhibited butyrate metabolism and caused the hydrogen partial pressure to increase to levels that would make syntrophic butyrate degradation via sulfate reduction energetically unfavorable (-5 to +3 kJ mol(-1) ). DNA extracted from the most probable number cultures and contaminated sediments contained sequences related to members of the families Syntrophomonadaceae and Syntrophaceae, whose members are known to syntrophically degrade fatty acids, as well as sequences related to uncultured Firmicutes, Desulfobulbaceae, Desulfobacteriaceae, and Desulfovibrionaceae. These data show that contaminated sediments degraded butyrate syntrophically coupled to methane production and sulfate reduction. 相似文献
962.
963.
Freeman ML Burkum CE Lanzer KG Jensen MK Ahmed M Yager EJ Flaño E Winslow GM Woodland DL Blackman MA 《Journal of immunology (Baltimore, Md. : 1950)》2011,187(12):6180-6184
CD4 T cells are essential for immune control of γ-herpesvirus latency. We previously identified a murine MHC class II-restricted epitope in γ-herpesvirus-68 gp150 (gp150(67-83)I-A(b)) that elicits CD4 T cells that are maintained throughout long-term infection. However, it is unknown whether naive cells can be recruited into the antiviral CD4 T cell pool during latency. In this study, we generate a mouse transgenic for a gp150-specific TCR and show epitope-specific activation of transgenic CD4 T cells during acute and latent infections. Furthermore, although only dendritic cells can stimulate virus-specific CD8 T cells during latency, we show that both dendritic cells and B cells stimulate transgenic CD4 T cells. These studies demonstrate that naive CD4 T cells specific for a viral glycoprotein can be stimulated throughout infection, even during quiescent latency, suggesting that CD4 T cell memory is maintained in part by the continual recruitment of naive cells. 相似文献
964.
Ryu SY Beutner G Kinnally KW Dirksen RT Sheu SS 《The Journal of biological chemistry》2011,286(24):21324-21329
Heart mitochondria utilize multiple Ca(2+) transport mechanisms. Among them, the mitochondrial ryanodine receptor provides a fast Ca(2+) uptake pathway across the inner membrane to control "excitation and metabolism coupling." In the present study, we identified a novel ryanodine-sensitive channel in the native inner membrane of heart mitochondria and characterized its pharmacological and biophysical properties by directly patch clamping mitoplasts. Four distinct channel conductances of ~100, ~225, ~700, and ~1,000 picosiemens (pS) in symmetrical 150 mm CsCl were observed. The 225 pS cation-selective channel exhibited multiple subconductance states and was blocked by high concentrations of ryanodine and ruthenium red, known inhibitors of ryanodine receptors. Ryanodine exhibited a concentration-dependent modulation of this channel, with low concentrations stabilizing a subconductance state and high concentrations abolishing activity. The 100, 700, and 1,000 pS conductances exhibited different channel characteristics and were not inhibited by ryanodine. Taken together, these findings identified a novel 225 pS channel as the native mitochondrial ryanodine receptor channel activity in heart mitoplasts with biophysical and pharmacological properties that distinguish it from previously identified mitochondrial ion channels. 相似文献
965.
966.
Singh U Raju B Lam S Zhou J Gadwood RC Ford CW Zurenko GE Schaadt RD Morin SE Adams WJ Friis JM Courtney M Palandra J Hackbarth CJ Lopez S Wu C Mortell KH Trias J Yuan Z Patel DV Gordeev MF 《Bioorganic & medicinal chemistry letters》2003,13(23):4209-4212
Combinatorial libraries of N-acylated 5-(S)-aminomethyloxazolidinone derivatives of S-oxide and S,S-dioxide tetrahydro-4(2H)-thiopyranyl and thiomorpholine phenyloxazolidinone series have been synthesized on a solid phase and evaluated for antimicrobial activity. Several novel potent leads have been identified, including orally active oxazolidinones with enhanced activity against respiratory tract infection pathogens Haemophilus influenzae and Moraxella catarrhalis. 相似文献
967.
Ping An Robert J. Straka Toni I. Pollin Mary F. Feitosa Mary K. Wojczynski E. Warwick Daw Jeffrey R. O’Connell Quince Gibson Kathleen A. Ryan Paul N. Hopkins Michael Y. Tsai Chao-Qiang Lai Michael A. Province Jose M. Ordovas Alan R. Shuldiner Donna K. Arnett Ingrid B. Borecki 《Human genetics》2014,133(7):919-930
Non-high-density lipoprotein cholesterol(NHDL) is an independent and superior predictor of CVD risk as compared to low-density lipoprotein alone. It represents a spectrum of atherogenic lipid fractions with possibly a distinct genomic signature. We performed genome-wide association studies (GWAS) to identify loci influencing baseline NHDL and its postprandial lipemic (PPL) response. We carried out GWAS in 4,241 participants of European descent. Our discovery cohort included 928 subjects from the Genetics of Lipid-Lowering Drugs and Diet Network Study. Our replication cohorts included 3,313 subjects from the Heredity and Phenotype Intervention Heart Study and Family Heart Study. A linear mixed model using the kinship matrix was used for association tests. The best association signal was found in a tri-genic region at RHOQ-PIGF-CRIPT for baseline NHDL (lead SNP rs6544903, discovery p = 7e?7, MAF = 2 %; validation p = 6e?4 at 0.1 kb upstream neighboring SNP rs3768725, and 5e?4 at 0.7 kb downstream neighboring SNP rs6733143, MAF = 10 %). The lead and neighboring SNPs were not perfect surrogate proxies to each other (D′ = 1, r 2 = 0.003) but they seemed to be partially dependent (likelihood ration test p = 0.04). Other suggestive loci (discovery p < 1e?6) included LOC100419812 and LOC100288337 for baseline NHDL, and LOC100420502 and CDH13 for NHDL PPL response that were not replicated (p > 0.01). The current and first GWAS of NHDL yielded an interesting common variant in RHOQ-PIGF-CRIPT influencing baseline NHDL levels. Another common variant in CDH13 for NHDL response to dietary high-fat intake challenge was also suggested. Further validations for both loci from large independent studies, especially interventional studies, are warranted. 相似文献
968.
969.
Paria Mirmonsef Anna L. Hotton Douglas Gilbert Derick Burgad Alan Landay Kathleen M. Weber Mardge Cohen Jacques Ravel Gregory T. Spear 《PloS one》2014,9(7)