A benzene-degrading nitrate-reducing microbial consortium displays aerobic and anaerobic benzene degradation pathways

All sequence data from this study were deposited at the European Bioinformatics Institute under the accession numbers ERS1670018 to ERS1670023. Further, all assigned genes, taxonomy, function, sequences of contigs, genes and proteins can be found in Table S3.In this study, we report transcription of genes involved in aerobic and anaerobic benzene degradation pathways in a benzene-degrading denitrifying continuous culture. Transcripts associated with the family Peptococcaceae dominated all samples (2136% relative abundance) indicating their key role in the community. We found a highly transcribed gene cluster encoding a presumed anaerobic benzene carboxylase (AbcA and AbcD) and a benzoate-coenzyme A ligase (BzlA). Predicted gene products showed >96% amino acid identity and similar gene order to the corresponding benzene degradation gene cluster described previously, providing further evidence for anaerobic benzene activation via carboxylation. For subsequent benzoyl-CoA dearomatization, bam-like genes analogous to the ones found in other strict anaerobes were transcribed, whereas gene transcripts involved in downstream benzoyl-CoA degradation were mostly analogous to the ones described in facultative anaerobes. The concurrent transcription of genes encoding enzymes involved in oxygenase-mediated aerobic benzene degradation suggested oxygen presence in the culture, possibly formed via a recently identified nitric oxide dismutase (Nod). Although we were unable to detect transcription of Nod-encoding genes, addition of nitrite and formate to the continuous culture showed indication for oxygen production. Such an oxygen production would enable aerobic microbes to thrive in oxygen-depleted and nitrate-containing subsurface environments contaminated with hydrocarbons.This study was supported by a grant of BE-Basic-FES funds from the Dutch Ministry of Economic Affairs. The research of A.J.M. Stams is supported by an ERC grant (project 323009) and the gravitation grant “Microbes for Health and Environment” (project 024.002.002) of the Netherlands Ministry of Education, Culture and Science. F. Hugenholtz was supported by the same gravitation grant (project 024.002.002). B. Hornung is supported by Wageningen University and the Wageningen Institute for Environment and Climate Research (WIMEK) through the IP/OP program Systems Biology (project KB-17-003.02-023).info:eu-repo/semantics/publishedVersio

I'll never forgive you: High conflict divorce, social network, and co-parenting conflicts

Contains fulltext : 177372.pdf (Publisher’s version ) (Open Access)The relation between divorce, co-parenting conflicts, and children's adjustment problems has been well established. An unresolved question for research and clinical interventions, however, is how conflicts between parents are maintained and/or escalate. This cross-sectional research tested the hypothesis that co-parenting conflicts in divorced couples are associated with perceived social network disapproval and that this relation is mediated by parents' tendency to forgive each other. In Study 1, a convenience sample of 136 divorced parents recruited via online forums, we showed that perceived social network disapproval was indeed positively related to co-parenting conflicts and that parents'tendency to forgive the other parent - albeit partly - explained this relationship. Strength of 0our research is that in Study 2, 110 parents referred to children's mental health care because the wellbeing of the children was severely compromised by the severity of the conflicts between parents, we replicated these results. In both studies perceived social network disapproval and co-parenting conflicts were positively related and this link was mediated by forgiveness: perceived social network disapproval was negatively related to forgiveness, which in turn was negatively related to more parental conflicts.12 p

NF-kappaB, AP-1, Zinc-deficiency and aging.

International audienceZinc (Zn) deficiency, a frequent condition in human population especially in aged persons, induces oxidative stress and subsequently activates/inhibits oxidant-sensitive transcription factors that can affect cell function, proliferation and survival leading to disease. Zn deficiency-triggered oxidative stress could affect cell signalling, including transcription factors containing Zn finger motifs and other oxidant-sensitive transcription factors such as nuclear factor kappa B (NF-kappaB) and activator protein-1 (AP-1). AP-1 can be activated in Zn deficiency that can occur secondary to an increase in cellular H(2)O(2), followed by activation of MAPKs p38 and JNK. Similarly, the cytosolic steps of the NF-kappaB cascade are activated by oxidants in Zn deficiency. However, an impaired nuclear transport of the active transcription factor leads to a low expression of NF-kappaB-dependent genes that could be involved in multiple steps of Zn deficiency associated pathology. We present here evidence that, following experimental depletion of Zn, both NF-kappaB and AP-1 signallings are altered in primary T cells isolated from young and elderly healthy individuals under CD3/CD28 costimulation. A supplementation of Zn restored both NF-kappaB and AP-1 activation in CD3/CD28 costimulated T cells from young, but not from elderly, healthy individuals, indicating that the Zn deficiency is only one component of a more complex mechanism involved in immunosenescence. In this review we summarize our present knowledge on NF-kappaB and AP-1 activation and underline the role of Zn in this process, especially in the context of Zn deficiency observed in aged persons leading to immunosenescence

HDL and atherothrombotic vascular disease

High-density lipoproteins (HDLs) exert many beneficial effects which may help to protect against the development or progression of atherosclerosis or even facilitate lesion regression. These activities include promoting cellular cholesterol efflux, protecting low-density lipoproteins (LDLs) from modification, preserving endothelial function, as well as anti-inflammatory and antithrombotic effects. However, questions remain about the relative importance of these activities for atheroprotection. Furthermore, the many molecules (both lipids and proteins) associated with HDLs exert both distinct and overlapping activities, which may be compromised by inflammatory conditions, resulting in either loss of function or even gain of dysfunction. This complexity of HDL functionality has so far precluded elucidation of distinct structure-function relationships for HDL or its components. A better understanding of HDL metabolism and structure-function relationships is therefore crucial to exploit HDLs and its associated components and cellular pathways as potential targets for anti-atherosclerotic therapies and diagnostic markers