Characterization of 1,4-Dioxane Biodegradation by a Microbial Community

In this study, a microbial community of bacteria was investigated for 1,4-dioxane(1,4-D) biodegradation. The enriched culture was investigated for 1,4-dioxane mineralization, co-metabolism of 1,4-dioxane and extra carbon sources, and characterized 1,4-dioxane biodegradation kinetics. The mineralization test indicates that the enriched culture was able to degrade 1,4-dioxane as the sole carbon and energy source. Interestingly, the distribution of 1,4-dioxane into the final biodegrading products were 36.9% into biomass, 58.3% completely mineralized to CO2, and about 4% escaped as VOC. The enriched culture has a high affinity with 1,4-dioxane during biodegradation. The kinetic coefficients of the Monod equation were qmax = 0.0063 mg 1,4-D/mg VSS/h, Ks = 9.42 mg/L, YT = 0.43 mg VSS/mg 1,4-dioxane and the decay rate was kd = 0.023 mg/mg/h. Tetrahydrofuran (THF) and ethylene glycol were both consumed together with 1,4-dioxane by the enriched culture; however, ethylene glycol did not show any influence on 1,4-dioxane biodegradation, while THF proved to be a competitive.

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Characterization of the Microbial Community and Culturable Denitrifying Bacteria in a Solid-phase Denitrification Process Using Poly(ε-caprolactone) as the Carbon and Energy Source

Microbes and Environments ◽

10.1264/jsme2.20.25 ◽

2005 ◽

Vol 20 (1) ◽

pp. 25-33 ◽

Cited By ~ 31

Author(s):

Yoko Horiba ◽

Shams Tabrez Khan ◽

Akira Hiraishi

Keyword(s):

Energy Source ◽

Microbial Community ◽

Solid Phase ◽

Denitrifying Bacteria ◽

Denitrification Process

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Characterization of a Mode of Specific Binding of Fibrin Monomer through its Amino-Terminal Domain by Macrophages and Macrophage Cell-Lines

Thrombosis and Haemostasis ◽

10.1055/s-0038-1645194 ◽

1990 ◽

Vol 63 (02) ◽

pp. 193-203 ◽

Cited By ~ 9

Author(s):

John R Shainoff ◽

Deborah J Stearns ◽

Patricia M DiBello ◽

Youko Hishikawa-Itoh

Keyword(s):

Peritoneal Macrophages ◽

Affinity Binding ◽

Macrophage Cell ◽

High Affinity Binding ◽

Amino Terminal ◽

High Affinity ◽

Terminal Domain ◽

Weak Binding ◽

Amino Terminal Domain

SummaryThe studies reported here probe the existence of a receptor-mediated mode of fibrin-binding by macrophages that is associated with the chemical change underlying the fibrinogen-fibrin conversion (the release of fibrinopeptides from the amino-terminal domain) without depending on fibrin-aggregation. The question is pursued by 1) characterization of binding in relation to fibrinopeptide content of both the intact protein and the CNBr-fragment comprising the amino-terminal domain known as the NDSK of the protein, 2) tests of competition for binding sites, and 3) photo-affinity labeling of macrophage surface proteins. The binding of intact monomers of types lacking either fibrinopeptide A alone (α-fibrin) or both fibrinopeptides A and B (αβ-fibrin) by peritoneal macrophages is characterized as proceeding through both a fibrin-specific low density/high affinity (BMAX ≃ 200–800 molecules/cell, KD ≃ 10−12 M) interaction that is not duplicated with fibrinogen, and a non-specific high density/low affinity (BMAX ≥ 105 molecules/cell, KD ≥ 10−6 M) interaction equivalent to the weak binding of fibrinogen. Similar binding characteristics are displayed by monocyte/macrophage cell lines (J774A.1 and U937) as well as peritoneal macrophages towards the NDSK preparations of these proteins, except for a slightly weaker (KD ≃ 10−10 M) high-affinity binding. The high affinity binding of intact monomer is inhibitable by fibrin-NDSK, but not fibrinogen-NDSK. This binding appears principally dependent on release of fibrinopeptide-A, because a species of fibrin (β-fibrin) lacking fibrinopeptide-B alone undergoes only weak binding similar to that of fibrinogen. Synthetic Gly-Pro-Arg and Gly-His-Arg-Pro corresponding to the N-termini of to the α- and the β-chains of fibrin both inhibit the high affinity binding of the fibrin-NDSKs, and the cell-adhesion peptide Arg-Gly-Asp does not. Photoaffinity-labeling experiments indicate that polypeptides with elec-trophoretically estimated masses of 124 and 187 kDa are the principal membrane components associated with specifically bound fibrin-NDSK. The binding could not be up-regulated with either phorbol myristyl acetate, interferon gamma or ADP, but was abolished by EDTA and by lipopolysaccharide. Because of the low BMAX, it is suggested that the high-affinity mode of binding characterized here would be too limited to function by itself in scavenging much fibrin, but may act cooperatively with other, less limited modes of fibrin binding.

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Faculty Opinions recommendation of Molecular-phylogenetic characterization of microbial community imbalances in human inflammatory bowel diseases.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1112029.567996 ◽

2008 ◽

Author(s):

John Pemberton ◽

Stefan Holubar

Keyword(s):

Microbial Community ◽

Inflammatory Bowel Diseases ◽

Phylogenetic Characterization ◽

Bowel Diseases ◽

Molecular Phylogenetic ◽

Inflammatory Bowel

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Enrichment and characterization of an anaerobic methyl ethyl ketoxime degrading culture from an anoxic/anaerobic/aerobic activated sludge sequencing batch reactor

Water Science & Technology ◽

10.2166/wst.1998.0590 ◽

1998 ◽

Vol 37 (4-5) ◽

pp. 95-98 ◽

Cited By ~ 1

Author(s):

Nancy G. Love ◽

Mary E. Rust ◽

Kathy C. Terlesky

Keyword(s):

Energy Source ◽

Activated Sludge ◽

Electron Acceptor ◽

Sequencing Batch Reactor ◽

Enrichment Culture ◽

Batch Reactor ◽

Nitrification Inhibitor ◽

Time Frame ◽

Methyl Ethyl

An anaerobic enrichment culture was developed from an anoxic/anaerobic/aerobic activated sludge sequencing batch reactor using methyl ethyl ketoxime (MEKO), a potent nitrification inhibitor, as the sole carbon and energy source in the absence of molecular oxygen and nitrate. The enrichment culture was gradually fed decreasing amounts of biogenic organic compounds and increasing concentrations of MEKO over 23 days until the cultures metabolized the oxime as the sole carbon source; the cultures were maintained for an additional 41 days on MEKO alone. Turbidity stabilized at approximately 100 mg/l total suspended solids. Growth on selective media plates confirmed that the microorganisms were utilizing the MEKO as the sole carbon and energy source. The time frame required for growth indicated that the kinetics for MEKO degradation are slow. A batch test indicated that dissolved organic carbon decreased at a rate comparable to MEKO consumption, while sulfate was not consumed. The nature of the electron acceptor in anaerobic MEKO metabolism is unclear, but it is hypothesized that the MEKO is hydrolyzed intracellularly to form methyl ethyl ketone and hydroxylamine which serve as electron donor and electron acceptor, respectively.

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Characterization of cellulose biodegradation kinetics in wastewater in view of increasing a WRRF’s capacity by a pre-treatment sieve step

Proceedings of the Water Environment Federation ◽

10.2175/193864717822156055 ◽

2017 ◽

Vol 2017 (7) ◽

pp. 4255-4262

Author(s):

Elena Torfs ◽

Julie Doucet ◽

Domenico Santoro ◽

Dang Ho ◽

Medhavi Gupta ◽

...

Keyword(s):

Biodegradation Kinetics ◽

Pre Treatment

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Acid-Sensing Ion Channels

The Oxford Handbook of Neuronal Ion Channels ◽

10.1093/oxfordhb/9780190669164.013.12 ◽

2020 ◽

Author(s):

Stefan Gründer

Keyword(s):

Nervous System ◽

Ion Channels ◽

Excitatory Synapses ◽

Detailed Characterization ◽

High Affinity ◽

Acid Sensing Ion Channels ◽

Long Time ◽

Pathological Pain

Acid-sensing ion channels (ASICs) are proton-gated Na+ channels. Being almost ubiquitously present in neurons of the vertebrate nervous system, their precise function remained obscure for a long time. Various animal toxins that bind to ASICs with high affinity and specificity have been tremendously helpful in uncovering the role of ASICs. We now know that they contribute to synaptic transmission at excitatory synapses as well as to sensing metabolic acidosis and nociception. Moreover, detailed characterization of mouse models uncovered an unanticipated role of ASICs in disorders of the nervous system like stroke, multiple sclerosis, and pathological pain. This review provides an overview on the expression, structure, and pharmacology of ASICs plus a summary of what is known and what is still unknown about their physiological functions and their roles in diseases.

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