A comparison of microsatellite instability in early onset gastric carcinomas from relatively low and high incidence European populations.

We have investigated the genetic basis of gastric carcinomas occurring in patients aged under 40 years from a Portuguese population with a relatively high incidence of gastric cancer. We analysed a panel of 12 microsatellite loci in DNA extracted from gastric carcinomas arising in 16 patients aged 24-39 years from Braga, Portugal. Overall, microsatellite instability (MI) in at least 1 locus was detected in 44% (7 of 16) of carcinomas. A single patient demonstrated a mutator phenotype suggestive of the hereditary nonpolyposis colorectal cancer syndrome with instability in 82% of loci. This carcinoma showed loss of expression of the hMLH1 mismatch repair protein. In a previous study, we found no evidence of MI among 10 cases of early onset gastric carcinomas from an English population, which has a relatively low incidence of gastric cancer. Comparing the 2 series, we found that there was a significant difference (p = 0.04) in the prevalence of MI (at least 1 marker affected). This geographical difference in low-level MI may be related to a significantly higher prevalence of background chronic atrophic gastritis (8 of 16 vs. 0 of 8) and Helicobacter pylori infection (15 of 16 vs. 2 of 8) in Portuguese carcinomas compared with English cases. Genetic mechanisms underlying the hereditary non-polyposis colorectal cancer syndrome may play a role in a small number of early onset gastric carcinomas. The difference in prevalence of low-level MI between these relatively high and low incidence European populations requires further investigation

Cityscapes without figures: geophysics, computing and the future of urban studies

Ye

Corrigendum to: Effects of exercise on adolescent and adult hypothalamic and hippocampal neuroinflammation (Hippocampus, (2016), 26, (1435–1446), 10.1002/hipo22620)

© 2018 Wiley Periodicals, Inc. Published in Hippocampus 26:1435–1446 (2016) DOI: 10.1002/hipo22620 The authors of this article have notified us that one of the funding agencies was incorrectly acknowledged. The correct citation of the funding body is listed below: This work was supported by a Discovery Project Grant (DP130100508) and a Future Fellowship (FT110100084) from the Australian Research Council as well as an RMIT University Vice Chancellor's Senior Research Fellowship. We apologize for any inconvenience this may have caused

Effects of exercise on adolescent and adult hypothalamic and hippocampal neuroinflammation.

Adolescence is a period of significant brain plasticity that can be affected by environmental factors, including the degree of physical activity. Here we hypothesized that adolescent rats would be more sensitive to the beneficial metabolic and anti-inflammatory effects of voluntary exercise than adult rats, whose more mature brains have less capacity for plasticity. We tested this by giving adolescent and adult Wistar rats four weeks' voluntary access to running wheels. At the end of this period we assessed metabolic effects, including weight and circulating leptin and ghrelin, as well as performance in a novel object recognition test of memory and central changes in neuronal proliferation, survival, synaptic density, and inflammatory markers in hippocampus. We found exercise reduced fat mass and circulating leptin levels in both adults and adolescents but suppressed total weight gain and lean mass in adults only. Exercise stimulated neuronal proliferation in the suprapyramidal blade of the dentate gyrus in both adults and adolescents without altering the number of mature neurons during this time frame. Exercise also increased dentate microglial numbers in adolescents alone and microglial numbers in this region were inversely correlated with performance in the novel object recognition test. Together these data suggest that adolescent hippocampal microglia are more sensitive to the effects of exercise than those of adults, but this leads to no apparent improvement in recognition memory. This article is protected by copyright. All rights reserved

A restatement of the natural science evidence concerning catchment-based ‘natural’ flood management in the UK

Flooding is a very costly natural hazard in the UK and is expected to increase further under future climate change scenarios. Flood defences are commonly deployed to protect communities and property from flooding, but in recent years flood management policy has looked towards solutions that seek to mitigate flood risk at flood-prone sites through targeted interventions throughout the catchment, sometimes using techniques which involve working with natural processes. This paper describes a project to provide a succinct summary of the natural science evidence base concerning the effectiveness of catchment-based ‘natural’ flood management in the UK. The evidence summary is designed to be read by an informed but not technically specialist audience. Each evidence statement is placed into one of four categories describing the nature of the underlying information. The evidence summary forms the appendix to this paper and an annotated bibliography is provided in the electronic supplementary material

A restatement of the natural science evidence concerning catchment-based "natural” flood management in the United Kingdom

Flooding is a very costly natural hazard in Great Britain and is expected to increase further under future climate change scenarios. Flood defences are commonly deployed to protect communities and property from flooding, but in recent years flood management policy has looked towards solutions that seek to mitigate flood risk at flood-prone sites through targeted interventions throughout the catchment, sometimes using techniques which involve working with natural processes. This paper describes a project to provide a succinct summary of the natural science evidence base concerning the effectiveness of catchment-based “natural” flood management in the United Kingdom. The evidence summary is designed to be read by an informed but not technically-specialist audience. Each evidence statement is placed into one of four categories describing the nature of the underlying information. The evidence summary forms the appendix to this paper and an annotated bibliography is provided in the electronic supplementary material

Analysis of the effects of depression associated polymorphisms on the activity of the BICC1 promoter in amygdala neurones

ACKNOWLEDGMENTS This work was funded by The BBSRC (BB/D004659/1) the Wellcome Trust (080980/Z/06/Z) and the Medical Research Council (G0701003).Peer reviewedPublisher PD