The influence of riparian woodland on the spatial and temporal variability of stream water temperatures in an upland salmon stream

International audienceThe spatio-temporal variability of stream water temperatures was investigated at six locations on the Girnock Burn (30km2 catchment), Cairngorms, Scotland over three hydrological years between 1998 and 2002. The key site-specific factors affecting the hydrology and climatology of the sampling points were investigated as a basis for physical process inference. Particular emphasis was placed on assessing the effects of riparian forest in the lower catchment versus the heather moorland riparian zones that are spatially dominant in the upper catchment. The findings were related to river heat budget studies that provided process detail. Gross changes in stream temperature were affected by the annual cycle of incoming solar radiation and seasonal changes in hydrological and climatological conditions. Inter-annual variation in these controlling variables resulted in inter-annual variability in thermal regime. However, more subtle inter-site differences reflected the impact of site-specific characteristics on various components of the river energy budget. Inter-site variability was most apparent at shorter time scales, during the summer months and for higher stream temperatures. Riparian woodland in the lower catchment had a substantial impact on thermal regime, reducing diel variability (over a period of 24 hours) and temperature extremes. Observed inter-site differences are likely to have a substantial effect on freshwater ecology in general and salmonid fish in particular. Keywords: temperature, thermal regime, forest, salmon, hydrology, Girnock Burn, Cairngor

Embodying compassion: A systematic review of the views of nurses and patients

© 2018 John Wiley & Sons Ltd Aims and objectives: To provide a review of empirical research investigating how compassion is expressed by nurses and received by patients in hospital settings. Background: Compassion is viewed as an important and fundamental part of a health professional practice. Universally, reports from both media and government agencies have addressed perceived deficits of compassion in healthcare with nurses accused of a lack of compassion. Research into compassion to date has largely focused on the problematic nature of compassion such as burnout, fatigue and other negative personal and work-related outcomes. Design: A systematic literature review of empirical research guided by a meta-ethnographic approach supported the systematic comparison and translation of the included studies. Six online databases were searched from January 2006–December 2016. Methods: This review was carried out according to the PRISMA-P reporting guidelines. How compassion in healthcare was defined was extracted alongside findings on how compassion was expressed by nurses and received by patients. Synthesis of the research was completed resulting in new interpretations. Results: Eleven papers met the inclusion criteria and were included in the review. Multiple differing definitions of compassion in healthcare were applied. Nurses embody and enact compassion through behaviours such as spending time with patients and communicating effectively with patients. Patients experience compassion through a sense of togetherness with nurses. Conclusion: Existing research demonstrated dissonance between the expression of compassion by nurses and how compassion is experienced by patients. The themes identified in this review should be considered by health professionals providing patient care. Relevance to clinical practice: Health providers should acknowledge and account for the time that nurses need with patients to demonstrate compassion in practice. Nursing education relating to the expression of compassion should articulate both the subjectivity and ambiguity of the term and examine the relationship between compassion and suffering

Nicotinamide mononucleotide (NMN) supplementation ameliorates the impact of maternal obesity in mice: comparison with exercise

Maternal overnutrition increases the risk of long-term metabolic dysfunction in offspring. Exercise improves metabolism partly by upregulating mitochondrial biogenesis or function, via increased levels of nicotinamide adenine dinucleotide (NAD+). We have shown that the NAD+ precursor, nicotinamide mononucleotide (NMN) can reverse some of the negative consequences of high fat diet (HFD) consumption. To investigate whether NMN can impact developmentally-set metabolic deficits, we compared treadmill exercise and NMN injection in offspring of obese mothers. Five week old lean and obese female C57BL6/J mice were mated with chow fed males. Female offspring weaned onto HFD were given treadmill exercise for 9 weeks, or NMN injection daily for 18 days. Maternal obesity programmed increased adiposity and liver triglycerides, with decreased glucose tolerance, liver NAD+ levels and citrate synthase activity in offspring. Both interventions reduced adiposity, and showed a modest improvement in glucose tolerance and improved markers of mitochondrial function. NMN appeared to have stronger effects on liver fat catabolism (Hadh) and synthesis (Fasn) than exercise. The interventions appeared to exert the most global benefit in mice that were most metabolically challenged (HFD-consuming offspring of obese mothers). This work encourages further study to confirm the suitability of NMN for use in reversing metabolic dysfunction linked to programming by maternal obesity

Mapping genomic and transcriptomic alterations spatially in epithelial cells adjacent to human breast carcinoma.

Almost all genomic studies of breast cancer have focused on well-established tumours because it is technically challenging to study the earliest mutational events occurring in human breast epithelial cells. To address this we created a unique dataset of epithelial samples ductoscopically obtained from ducts leading to breast carcinomas and matched samples from ducts on the opposite side of the nipple. Here, we demonstrate that perturbations in mRNA abundance, with increasing proximity to tumour, cannot be explained by copy number aberrations. Rather, we find a possibility of field cancerization surrounding the primary tumour by constructing a classifier that evaluates where epithelial samples were obtained relative to a tumour (cross-validated micro-averaged AUC = 0.74). We implement a spectral co-clustering algorithm to define biclusters. Relating to over-represented bicluster pathways, we further validate two genes with tissue microarrays and in vitro experiments. We highlight evidence suggesting that bicluster perturbation occurs early in tumour development

Redistribution of H3K27me3 upon DNA hypomethylation results in de-repression of Polycomb target genes

BACKGROUND: DNA methylation and the Polycomb repression system are epigenetic mechanisms that play important roles in maintaining transcriptional repression. Recent evidence suggests that DNA methylation can attenuate the binding of Polycomb protein components to chromatin and thus plays a role in determining their genomic targeting. However, whether this role of DNA methylation is important in the context of transcriptional regulation is unclear. RESULTS: By genome-wide mapping of the Polycomb Repressive Complex 2-signature histone mark, H3K27me3, in severely DNA hypomethylated mouse somatic cells, we show that hypomethylation leads to widespread H3K27me3 redistribution, in a manner that reflects the local DNA methylation status in wild-type cells. Unexpectedly, we observe striking loss of H3K27me3 and Polycomb Repressive Complex 2 from Polycomb target gene promoters in DNA hypomethylated cells, including Hox gene clusters. Importantly, we show that many of these genes become ectopically expressed in DNA hypomethylated cells, consistent with loss of Polycomb-mediated repression. CONCLUSIONS: An intact DNA methylome is required for appropriate Polycomb-mediated gene repression by constraining Polycomb Repressive Complex 2 targeting. These observations identify a previously unappreciated role for DNA methylation in gene regulation and therefore influence our understanding of how this epigenetic mechanism contributes to normal development and disease

Genetic, environmental and stochastic factors in monozygotic twin discordance with a focus on epigenetic differences

PMCID: PMC3566971This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited

Identification of tammar wallaby SIRH12, derived from a marsupial-specific retrotransposition event

In humans and mice, there are 11 genes derived from sushi-ichi related retrotransposons, some of which are known to play essential roles in placental development. Interestingly, this family of retrotransposons was thought to exist only in eutherian mammals, indicating their significant contributions to the eutherian evolution, but at least one, PEG10, is conserved between marsupials and eutherians. Here we report a novel sushi-ichi retrotransposon-derived gene, SIRH12, in the tammar wallaby, an Australian marsupial species of the kangaroo family. SIRH12 encodes a protein highly homologous to the sushi-ichi retrotransposon Gag protein in the tammar wallaby, while SIRH12 in the South American short-tailed grey opossum is a pseudogene degenerated by accumulation of multiple nonsense mutations. This suggests that SIRH12 retrotransposition occurred only in the marsupial lineage but acquired and retained some as yet unidentified novel function, at least in the lineage of the tammar wallaby

Sequences Sufficient for Programming Imprinted Germline DNA Methylation Defined

Epigenetic marks are fundamental to normal development, but little is known about signals that dictate their placement. Insights have been provided by studies of imprinted loci in mammals, where monoallelic expression is epigenetically controlled. Imprinted expression is regulated by DNA methylation programmed during gametogenesis in a sex-specific manner and maintained after fertilization. At Rasgrf1 in mouse, paternal-specific DNA methylation on a differential methylation domain (DMD) requires downstream tandem repeats. The DMD and repeats constitute a binary switch regulating paternal-specific expression. Here, we define sequences sufficient for imprinted methylation using two transgenic mouse lines: One carries the entire Rasgrf1 cluster (RC); the second carries only the DMD and repeats (DR) from Rasgrf1. The RC transgene recapitulated all aspects of imprinting seen at the endogenous locus. DR underwent proper DNA methylation establishment in sperm and erasure in oocytes, indicating the DMD and repeats are sufficient to program imprinted DNA methylation in germlines. Both transgenes produce a DMD-spanning pit-RNA, previously shown to be necessary for imprinted DNA methylation at the endogenous locus. We show that when pit-RNA expression is controlled by the repeats, it regulates DNA methylation in cis only and not in trans. Interestingly, pedigree history dictated whether established DR methylation patterns were maintained after fertilization. When DR was paternally transmitted followed by maternal transmission, the unmethylated state that was properly established in the female germlines could not be maintained. This provides a model for transgenerational epigenetic inheritance in mice