Biological Records Centre Annual Report 2005-2006

The period covered by this report is the first year of a new six-year partnership between CEH and JNCC. For this period, there is increased emphasis on targeted survey, on analysis and interpretation and on communications and outreach. These activities were always part of BRC’s work, but they have been given greater prominence as a result of rapid developments in information technology. Data are increasingly reaching BRC in electronic form, so that the effort of data entry and collation is reduced. The data, collected by many volunteers and then collated and analysed at BRC, document the changing status and distribution of plants and animals in Britain. Distribution maps are published in atlases and are available via the internet through the NBN Gateway. The effects of change or loss of habitats, the influence of climate change and the consequences of changing water quality are all examples of the environmental factors that affect our biodiversity and which BRC aims to document and understand. The results are vital for developing environmental policies, to support conservation, and for fundamental ecological research. BRC is funded jointly by JNCC and NERC through a partnership based on a Memorandum of Agreement (MoA). The partnership started in 1973 when the Nature Conservancy was divided to form the successor bodies Nature Conservancy Council (NCC) and Institute of Terrestrial Ecology (ITE). NCC was in turn divided further to form JNCC and three Country Agencies, while ITE was merged with other NERC units to form CEH. Through all these changes, the partnership has been maintained. A six-year memorandum of agreement ended on 31 January 2005 (Hill et al. 2005). The present report covers the first full year, 2005-6, of the new agreement for 2005-2010. Rapid progress in information technology continues to be highly beneficial for BRC, whose data are increasingly used by the UK country conservation agencies, environmental consultants, NGOs, research workers, policy makers and volunteers. It is gratifying to know that, through our ability to display data on the National Biodiversity Network (NBN) Gateway, some of our data suppliers now have immediate access to their own data in a convenient form. The year 2005-6 has been one of steady progress, with new datasets added to BRC, substantial additions to existing data, and improved communication with the NBN Gateway. The most high profile activity of the year has been the Harlequin Ladybird Survey, which has enabled us to observe the early stages of colonization by a mobile insect in greater detail than has been possible in any previous case

J-Band Infrared Spectroscopy of a Sample of Brown Dwarfs Using Nirspec on Keck II

Near-infrared spectroscopic observations of a sample of very cool, low-mass objects are presented with higher spectral resolution than in any previous studies. Six of the objects are L-dwarfs, ranging in spectral class from L2 to L8/9, and the seventh is a methane or T-dwarf. These new observations were obtained during commissioning of NIRSPEC, the first high-resolution near-infrared cryogenic spectrograph for the Keck II 10-meter telescope on Mauna Kea, Hawaii. Spectra with a resolving power of R=2500 from 1.135 to 1.360 microns (approximately J-band) are presented for each source. At this resolution, a rich spectral structure is revealed, much of which is due to blending of unresolved molecular transitions. Strong lines due to neutral potassium (K I), and bands due to iron hydride (FeH) and steam (H2O) change significantly throughout the L sequence. Iron hydride disappears between L5 and L8, the steam bands deepen and the K I lines gradually become weaker but wider due to pressure broadening. An unidentified feature occurs at 1.22 microns which has a temperature dependence like FeH but has no counterpart in the available FeH opacity data. Because these objects are 3-6 magnitudes brighter in the near-infrared compared to the I-band, spectral classification is efficient. One of the objects studied (2MASSW J1523+3014) is the coolest L-dwarf discovered so far by the 2-Micron All-Sky Survey (2MASS), but its spectrum is still significantly different from the methane-dominated objects such as Gl229B or SDSS 1624+0029.Comment: New paper, Latex format, 2 figures, accepted to ApJ Letter

The Gibbs-Thomson formula at small island sizes - corrections for high vapour densities

In this paper we report simulation studies of equilibrium features, namely circular islands on model surfaces, using Monte-Carlo methods. In particular, we are interested in studying the relationship between the density of vapour around a curved island and its curvature-the Gibbs-Thomson formula. Numerical simulations of a lattice gas model, performed for various sizes of islands, don't fit very well to the Gibbs-Thomson formula. We show how corrections to this form arise at high vapour densities, wherein a knowledge of the exact equation of state (as opposed to the ideal gas approximation) is necessary to predict this relationship. Exploiting a mapping of the lattice gas to the Ising model one can compute the corrections to the Gibbs-Thomson formula using high field series expansions. We also investigate finite size effects on the stability of the islands both theoretically and through simulations. Finally the simulations are used to study the microscopic origins of the Gibbs-Thomson formula. A heuristic argument is suggested in which it is partially attributed to geometric constraints on the island edge.Comment: 27 pages including 7 figures, tarred, gzipped and uuencoded. Prepared using revtex and espf.sty. To appear in Phys. Rev.

Enterohepatic Helicobacter in ulcerative colitis:Potential pathogenic entities?

Background: Changes in bacterial populations termed "dysbiosis" are thought central to ulcerative colitis (UC) pathogenesis. In particular, the possibility that novel Helicobacter organisms play a role in human UC has been debated but not comprehensively investigated. The aim of this study was to develop a molecular approach to investigate the presence of Helicobacter organisms in adults with and without UC.Methodology/Principal Findings: A dual molecular approach to detect Helicobacter was developed. Oligonucleotide probes against the genus Helicobacter were designed and optimised alongside a validation of published H. pylori probes. A comprehensive evaluation of Helicobacter genus and H. pylori PCR primers was also undertaken. The combined approach was then assessed in a range of gastrointestinal samples prior to assessment of a UC cohort. Archival colonic samples were available from 106 individuals for FISH analysis (57 with UC and 49 non-IBD controls). A further 118 individuals were collected prospectively for dual FISH and PCR analysis (86 UC and 32 non-IBD controls). An additional 27 non-IBD controls were available for PCR analysis. All Helicobacter PCR-positive samples were sequenced. The association between Helicobacter and each study group was statistically analysed using the Pearson Chi Squared 2 tailed test. Helicobacter genus PCR positivity was significantly higher in UC than controls (32 of 77 versus 11 of 59, p = 0.004). Sequence analysis indicated enterohepatic Helicobacter species prevalence was significantly higher in the UC group compared to the control group (30 of 77 versus 2 of 59, p&lt;0.0001). PCR and FISH results were concordant in 74 (67.9%) of subjects. The majority of discordant results were attributable to a higher positivity rate with FISH than PCR.Conclusions/Significance: Helicobacter organisms warrant consideration as potential pathogenic entities in UC. Isolation of these organisms from colonic tissue is needed to enable interrogation of pathogenicity against established criteria.</p

Subcellular Epithelial HMGB1 Expression Is Associated with Colorectal Neoplastic Progression, Male Sex, Mismatch Repair Protein Expression, Lymph Node Positivity, and an ‘Immune Cold’ Phenotype Associated with Poor Survival

Acknowledgments: The authors would like to thank NHS Grampian Biorepository, in particular Joan Wilson, Victoria Morrison, Kristine Nellany, and Nadine Hay, for their assistance in preparing tissue for this project. The authors also thank Tasneem O Atezia and Christina A Christopoulou for their contribution to this project during their time in the McLean laboratory. The laboratory work was instigated when M.H.M., R.J.P. and D.P.B. were based at the Institute of Medical Sciences, University of Aberdeen. Funding This work was funded by project grants from NHS Grampian Endowments and Friends of Anchor (https://www.friendsofanchor.org, charity no. SC025332). Within the McLean laboratory at the University of Aberdeen, SH received a Medical Research Scotland Summer Studentship, and AH received an Aberdeen Summer Research Studentship (University of Aberdeen).Peer reviewedPublisher PD

Fibroblast activation and inflammation in frozen shoulder

Introduction: Frozen shoulder is a common, fibro-proliferative disease characterised by the insidious onset of pain and progressively restricted range of shoulder movement. Despite the prevalence of this disease, there is limited understanding of the molecular mechanisms underpinning the pathogenesis of this debilitating disease. Previous studies have identified increased myofibroblast differentiation and proliferation, immune cell influx and dysregulated cytokine production. We hypothesised that subpopulations within the fibroblast compartment may take on an activated phenotype, thus initiating the inflammatory processes observed in frozen shoulder. Therefore, we sought to evaluate the presence and possible pathogenic role of known stromal activation proteins in Frozen shoulder, Methods: Shoulder capsule samples were collected from 10 patients with idiopathic frozen shoulder and 10 patients undergoing shoulder stabilisation surgery. Fibroblast activation marker expression (CD248, CD146, VCAM and PDPN, FAP) was quantified using immunohistochemistry. Control and diseased fibroblasts were cultured for in vitro studies from capsule biopsies from instability and frozen shoulder surgeries, respectively. The inflammatory profile and effects of IL-1β upon diseased and control fibroblasts was assessed using ELISA, immunohistochemistry and qPCR. Results: Immunohistochemistry demonstrated increased expression of fibroblast activation markers CD248, CD146, VCAM and PDPN in the frozen shoulder group compared with control (p &lt; 0.05). Fibroblasts cultured from diseased capsule produced elevated levels of inflammatory protein (IL-6, IL-8 &amp; CCL-20) in comparison to control fibroblasts. Exposing control fibroblasts to an inflammatory stimuli, (IL-1ß) significantly increased stromal activation marker transcript and protein expression (CD248, PDPN and VCAM). Conclusions: These results show that fibroblasts have an activated phenotype in frozen shoulder and this is associated with inflammatory cytokine dysregulation. Furthermore, it supports the hypothesis that activated fibroblasts may be involved in regulating the inflammatory and fibrotic processes involved in this disease

Colonic epithelial cathelicidin (LL-37) expression intensity is associated with progression of colorectal cancer and presence of CD8+ T cell infiltrate

Colorectal cancer (CRC) remains a leading cause of cancer mortality. Here, we define the colonic epithelial expression of cathelicidin (LL-37) in CRC. Cathelicidin exerts pleotropic effects including anti-microbial and immunoregulatory functions. Genetic knockout of cathelicidin led to increased size and number of colorectal tumours in the azoxymethane-induced murine model of CRC. We aimed to translate this to human disease. The expression of LL-37 in a large (n = 650) fully characterised cohort of treatment-naïve primary human colorectal tumours and 50 matched normal mucosa samples with associated clinical and pathological data (patient age, gender, tumour site, tumour stage [UICC], presence or absence of extra-mural vascular invasion, tumour differentiation, mismatch repair protein status, and survival to 18 years) was assessed by immunohistochemistry. The biological consequences of LL-37 expression on the epithelial barrier and immune cell phenotype were assessed using targeted quantitative PCR gene expression of epithelial permeability (CLDN2, CLDN4, OCLN, CDH1, and TJP1) and cytokine (IL-1β, IL-18, IL-33, IL-10, IL-22, and IL-27) genes in a human colon organoid model, and CD3+ , CD4+ , and CD8+ lymphocyte phenotyping by immunohistochemistry, respectively. Our data reveal that loss of cathelicidin is associated with human CRC progression, with a switch in expression intensity an early feature of CRC. LL-37 expression intensity is associated with CD8+ T cell infiltrate, influenced by tumour characteristics including mismatch repair protein status. There was no effect on epithelial barrier gene expression. These data offer novel insights into the contribution of LL-37 to the pathogenesis of CRC and as a therapeutic molecule