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Aim Given the paucity of data on the distribution of habitats and species for most marine species, particularly those that are rare and in need of protection, there is a need to model species distributions. Using the fan mussel, Atrina fragilis (Pennant 1777), as our case species, the aim of the study was to predict new areas of occurrence for A. fragilis, estimate the extent of potentially suitable areas, determine the proportion of these areas that are included in the recently designated nature conservation MPAs off the west of Scotland and identify possible environmental drivers in the distribution of A. fragilis. Location West coast of Scotland, UK. Methods Using a point process framework, we modelled presence-only data, including historic records. A quadrat survey employing digital still photography was conducted in areas of high and low suitability to verify the model, and subsequently, a targeted survey was undertaken in areas predicted as highly suitable by the models using towed video cameras. Results Five environmental variables were of prime importance in explaining the distribution of A. fragilis. The results from the verification survey support model performance. Atrina fragilis was found in 80% of the targeted transects undertaken. Approximately 14% of the total area predicted as suitable for A. fragilis occurred within recently designated marine protected areas ( MPAs) indicating considerable potential for recolonization given suitable protection. Main conclusions The verified model suggests that limited presence-only and historical records of rare species can perform well within a SDM framework allowing the identification of further suitable areas. The prominence of bathymetric ruggedness in the models is unexpected, given the understood ecological niche for A. fragilis and pinnids in general, but is consistent with the fact that seabed topography can offer protection from fishing pressure. These results will inform restoration objectives of the MPA network. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Transected axons of the central nervous system fail to regenerate and instead die back away from the lesion site, resulting in permanent disability. Although both intrinsic (eg, microtubule instability, calpain activation) and extrinsic (ie, macrophages) processes are implicated in axonal dieback, the underlying mechanisms remain uncertain. Furthermore, the precise mechanisms that cause delayed 'bystander' loss of spinal axons, that is, ones that were not directly damaged by the initial insult, but succumbed to secondary degeneration, remain unclear. Our goal was to evaluate the role of intra-axonal Ca(2+) stores in secondary axonal degeneration following spinal cord injury. METHODS: We developed a 2-photon laser-induced spinal cord injury model to follow morphological and Ca(2+) changes in live myelinated spinal axons acutely following injury. RESULTS: Transected axons 'died back' within swollen myelin or underwent synchronous pan-fragmentation associated with robust Ca(2+) increases. Spared fibers underwent delayed secondary bystander degeneration. Reducing Ca(2+) release from axonal stores mediated by ryanodine and inositol triphosphate receptors significantly decreased axonal dieback and bystander injury. Conversely, a gain-of-function ryanodine receptor 2 mutant or pharmacological treatments that promote axonal store Ca(2+) release worsened these events. INTERPRETATION: Ca(2+) release from intra-axonal Ca(2+) stores, distributed along the length of the axon, contributes significantly to secondary degeneration of axons. This refocuses our approach to protecting spinal white matter tracts, where emphasis has been placed on limiting Ca(2+) entry from the extracellular space across cell membranes, and emphasizes that modulation of axonal Ca(2+) stores may be a key pharmacotherapeutic goal in spinal cord injury. Ann Neurol 2014;75:220-229. [ABSTRACT FROM AUTHOR]

Objective Transected axons of the central nervous system fail to regenerate and instead die back away from the lesion site, resulting in permanent disability. Although both intrinsic (eg, microtubule instability, calpain activation) and extrinsic (ie, macrophages) processes are implicated in axonal dieback, the underlying mechanisms remain uncertain. Furthermore, the precise mechanisms that cause delayed 'bystander' loss of spinal axons, that is, ones that were not directly damaged by the initial insult, but succumbed to secondary degeneration, remain unclear. Our goal was to evaluate the role of intra-axonal Ca2+ stores in secondary axonal degeneration following spinal cord injury. Methods We developed a 2-photon laser-induced spinal cord injury model to follow morphological and Ca2+ changes in live myelinated spinal axons acutely following injury. Results Transected axons 'died back' within swollen myelin or underwent synchronous pan-fragmentation associated with robust Ca2+ increases. Spared fibers underwent delayed secondary bystander degeneration. Reducing Ca2+ release from axonal stores mediated by ryanodine and inositol triphosphate receptors significantly decreased axonal dieback and bystander injury. Conversely, a gain-of-function ryanodine receptor 2 mutant or pharmacological treatments that promote axonal store Ca2+ release worsened these events. Interpretation Ca2+ release from intra-axonal Ca2+ stores, distributed along the length of the axon, contributes significantly to secondary degeneration of axons. This refocuses our approach to protecting spinal white matter tracts, where emphasis has been placed on limiting Ca2+ entry from the extracellular space across cell membranes, and emphasizes that modulation of axonal Ca2+ stores may be a key pharmacotherapeutic goal in spinal cord injury. Ann Neurol 2014;75:220-229 [ABSTRACT FROM AUTHOR]

Myelin-derived molecules inhibit axonal regeneration in the CNS. The Long–Evans Shaker rat is a naturally occurring dysmyelinated mutant, which although able to express the components of myelin lacks functional myelin in adulthood. Given that myelin breakdown exposes axons to molecules that are inhibitory to regeneration, we sought to determine whether injured dorsal column axons in a Shaker rat would exhibit a regenerative response absent in normally myelinated Long–Evans (control) rats. Although Shaker rat axons did not regenerate beyond the lesion, they remained at the caudal end of the crush site. Control rat axons, in contrast, retracted and died back from the edge of the crush. The absence of retraction/dieback in Shaker rats was associated with a reduced phagocytic reaction to dorsal column crush around the caudal edge of the lesion. Systemic injection of minocycline, a tetracycline derivative, in control rats reduced both the macrophage response and axonal retraction/dieback following dorsal column injury. In contrast, increasing macrophage activation by spinal injection of the yeast particulate zymosan had no effect on axonal retraction/dieback in Shaker rats. Schwann cell invasion was reduced in minocycline-treated control rats compared with untreated control rats, and was almost undetectable in Shaker rats, suggesting that like axonal retraction/dieback, spinal Schwann cell infiltration is dependent upon macrophage-mediated myelin degeneration. These results indicate that following spinal cord injury the phagocyte-mediated degeneration of myelin and subsequent exposure of inhibitory molecules to the injured axons contributes to their retraction/dieback. [ABSTRACT FROM AUTHOR]

Presents a literature review on interleukin 6 (IL-6) and haemostasis. Significance of IL-6 in the treatment of haemostasis; Information on IL-6 and its receptors; Coverage of the IL-6 cytokine family.

Coagulation factor concentrates are known to inhibit a variety of immune reactions when assessed in vitro. This study assessed the immunomodulatory activity of a wide range of coagulation factor concentrates by measuring their inhibition of PHA-stimulated lymphocyte proliferation and reduction in IL-2 secretion. The hypothesis that TGF-β is responsible for most of these effects was tested by measuring biologically active TGF-β and immunoreactive TGF-β1 in the concentrates and comparing the levels recorded with immunosuppressive activity. In addition, the coagulation factors were compared directly with a standard preparation of TGF-β in a TGF-β-specific bioassay and in lymphocyte proliferation assays. Although there was a broad correlation between levels of total or active TGF-β and immunosuppressive activity across all of the coagulation factors tested, individual data sets showed clear discrepancies. Implying that TGF-β probably serves as a surrogate marker for other immunomodulatory contaminants and that neither TGF-β nor any other single substance could account for all of the immunosuppressive activity observed. Furthermore, there was a difference of more than 100-fold in the relative potencies of coagulation factors and pure TGF-β, when compared in immunosuppression assays, indicating that the different assays did not measure the same substance. Whereas anti-TGF-β antibody almost completely blocked the activity of coagulation factor concentrates (TGF-β-specific bioassay) and abrogated the effect of authentic TGF-β (immunosuppression assays) at high concentrations it achieved <50% reversal of the immunosuppressive effects of coagulation factors in immunosuppression assays. These findings indicated that TGF-β accounted for only a minor proportion of the immunosuppressive activity in most coagulation factor concentrates. [ABSTRACT FROM AUTHOR]

1. The methane mono-oxygenase from Methylosinus trichosporium OB3b was soluble. The only suitable electron donor was NAD(P)H, neither sodium L-ascorbate nor electrons derived from the oxidation of methanol could substitute for NAD(P)H. Evidence is presented for the existence of an NAD+-linked formaldehyde dehydrogenase. 2. Monooxygenase activity was not inhibited by a range of potential inhibitors including potassium cyanide, amytal, carbon monoxide or various metal-chelating agents, although 8-hydroxy-quinoline and ethyne were effective in this respect. 3. Although the enzyme preparations were unstable on storage, the crude extract could be resolved into two components by ion-exchange chromatography. Activity could be restored to one of the components on addition of purified components from Methylococcus capsulatus (Bath). 4. Cross-reactivity of mono-oxygenase components and other similarities between the enzymes from M. trichosporium and M. capsulatus are discussed. The properties of the M. trichosporium methane mono-oxygenase reported here are contrasted with the properties of the same enzyme reported by others. [ABSTRACT FROM AUTHOR]

CellProfiler is a widely used software for creating reproducible, reusable image analysis workflows without needing to code. In addition to the >90 modules that make up the main CellProfiler program, CellProfiler has a plugins system that allows for the creation of new modules which integrate with other Python tools or tools that are packaged in software containers. The CellProfiler‐plugins repository contains a number of these CellProfiler modules, especially modules that are experimental and/or dependency‐heavy. Here, we present an upgraded CellProfiler‐plugins repository, an example of accessing containerised tools, improved documentation and added citation/reference tools to facilitate the use and contribution of the community. [ABSTRACT FROM AUTHOR]

ABSTRACT This paper reports an investigation into the effect of carbon dioxide (CO2) gas on various ultra wideband channel coefficients. Measurements were conducted using apparatus consisting of a rubberized tube (6 mm diameter) connected to a source of CO2 or nitrogen (N2). For support, the rubberized tube was wrapped twice around a PVC pipe (160 mm diameter). The rubberized tube was flushed with 100% CO2 several times before being sealed in the tube at atmospheric pressure. In between measurement trials, removal of CO2 was achieved by flushing with pure nitrogen. A Vector Network Analyzer (VNA) using two identical directional antennas, with the wrapped section of tubing placed in-between, measured the channel coefficients over ultra wideband frequency spans of (0.3-8) GHz and (1-2) GHz. Significant magnitude differences between the baseline condition and that of CO2 were observed. We found the same signature of difference curves over the same frequency spans for different measurements. Difference in shape in the frequency band of (1-2) GHz is the same as that of the measured difference over 1-2 GHz in entire frequency band of 300 MHz to 8 GHz for the measured channel coefficients. © 2016 Wiley Periodicals, Inc. Microwave Opt Technol Lett 58:1543-1546, 2016 [ABSTRACT FROM AUTHOR]

The blue skate (Dipturus batis) has a patchy distribution across the North‐East Atlantic Ocean, largely restricted to occidental seas around the British Isles following fisheries‐induced population declines and extirpations. The viability of remnant populations remains uncertain and could be impacted by continued fishing and by‐catch pressure, and the projected impacts of climate change. We genotyped 503 samples of D. batis, obtained opportunistically from the widest available geographic range, across 6 350 single nucleotide polymorphisms (SNPs) using a reduced‐representation sequencing approach. Genotypes were used to assess the species' contemporary population structure, estimate effective population sizes and identify putative signals of selection in relation to environmental variables using a seascape genomics approach. We identified genetic discontinuities between inshore (British Isles) and offshore (Rockall and Faroe Island) populations, with differentiation most pronounced across the deep waters of the Rockall Trough. Effective population sizes were largest in the Celtic Sea and Rockall, but low enough to be of potential conservation concern among Scottish and Faroese sites. Among the 21 candidate SNPs under positive selection was one significantly correlated with environmental variables predicted to be affected by climate change, including bottom temperature, salinity and pH. The paucity of well‐annotated elasmobranch genomes precluded us from identifying a putative function for this SNP. Nevertheless, our findings suggest that climate change could inflict a strong selective force upon remnant populations of D. batis, further constraining its already‐restricted habitat. Furthermore, the results provide fundamental insights on the distribution, behaviour and evolutionary biology of D. batis in the North‐East Atlantic that will be useful for the establishment of conservation actions for this and other critically endangered elasmobranchs. [ABSTRACT FROM AUTHOR]

Microparticles (MPs) are considered to be important biological effectors of several different physiological and pathological processes. There is increasing evidence of their role in haemostasis and thrombosis, and also of their importance in cancer cell survival, invasiveness and metastasis. The level of circulating MPs has been assessed in many different disease states, and there are reports that patients with malignancy and patients with thrombosis have increased levels of circulating MPs and MP-dependent thrombogenic potential. Research into the function and effect of MPs is currently hampered by a lack of standardization in the methods used to identify and quantify them. As these methods improve it is likely that MP assays will be of use both diagnostically and therapeutically in the future. [ABSTRACT FROM AUTHOR]

Monocytes and macrophages provide key targets for the action of novel anti-inflammatory therapeutics targeted at inhibition of PDE4 cAMP-specific phosphodiesterases. PDE4 enzymes provide the dominant cAMP phosphodiesterase activity in U937 human monocytic cells. Differentiation of U937 monocytic cells to a macrophage-like phenotype causes a marked reduction in total cellular PDE4 activity. Monocytic U937 cells express the long PDE4A4, PDE4D5 and PDE4D3 isoforms plus the short PDE4B2 isoform. Differentiation of U937 cells to a macrophage-like phenotype causes a marked downregulation of PDE4D3 and PDE4D5, elicits a marked upregulation of PDE4B2 and induces the novel PDE4A10 long isoform. Comparable patterns are found in human peripheral blood monocytes and macrophages differentiated from them. Immunopurification of PDE4 subfamilies identifies long PDE4D isoforms as providing the major PDE4 activity in U937 monocytic cells. In U937 macrophage-like cells, the activity of the short PDE4B2 isoform predominates. No indication of either the expression or induction of PDE4C was evident. Activation of ERK exerts an inhibitory effect on total PDE4 activity in monocytic U937 cells, where the activity of long PDE4 isoforms predominates. The effect of ERK activation is switched to one of overall stimulation of total PDE4 activity in macrophage U937 cells, where the activity of the short PDE4B2 isoform predominates.10 The profound differentiation-induced changes in PDE4 isoform profile identified here suggests that the development of inhibitors specific for particular PDE4 isoforms may allow for selective effects on monocytes and macrophages to be achieved. [ABSTRACT FROM AUTHOR]

The article focuses on a study showing occurrence of mutation in both calreticulin gene (CALR) and JAK2 V617F in a retrospective analysis of patients. Topics discussed include JAK 2 V617F and CALR exon 9 mutation considered to be mutually exclusive, whole genome analysis identified mutation of CALR gene in patients with thrombocythaemia and myelofibrosis, and a real time quantitative polymerase chain reaction plot for double-mutant patients.

ABSTRACT The sensory neurons innervating the urinary bladder and distal colon project to similar regions of the central nervous system and often are affected simultaneously by various diseases and disorders, including spinal cord injury. Anatomical and physiological commonalities between the two organs involve the participation of shared spinally derived pathways, allowing mechanisms of communication between the bladder and colon. Prior electrophysiological data from our laboratory suggest that the bladder also may receive sensory innervation from a nonspinal source through the vagus nerve, which innervates the distal colon as well. The present study therefore aimed to determine whether anatomical evidence exists for vagal innervation of the male rat urinary bladder and to assess whether those vagal afferents also innervate the colon. Additionally, the relative contribution to bladder and colon sensory innervation of spinal and vagal sources was determined. By using lipophilic tracers, neurons that innervated the bladder and colon in both the nodose ganglia (NG) and L6/S1 and L1/L2 dorsal root ganglia (DRG) were quantified. Some single vagal and spinal neurons provided dual innervation to both organs. The proportions of NG afferents labeled from the bladder did not differ from spinal afferents labeled from the bladder when considering the collective population of total neurons from either group. Our results demonstrate evidence for vagal innervation of the bladder and colon and suggest that dichotomizing vagal afferents may provide a neural mechanism for cross-talk between the organs. J. Comp. Neurol. 522:3667-3682, 2014. © 2014 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Objective: Failure of remyelination is a critical impediment to recovery in multiple sclerosis (MS). Chondroitin sulfate proteoglycans (CSPGs) have been reported to accumulate in MS lesions, and we thus examined the functional roles of CSPGs on oligodendrocyte precursor cells (OPCs), oligodendrocytes, and remyelination. Methods: We evaluated the expression of CSPGs in lysolecithin-injected mouse spinal cord, an animal model of demyelination and spontaneous remyelination. The functional impact of CSPGs on OPCs and remyelination was investigated using cultured adult murine and human OPCs and by treating demyelinated mice with xyloside to reduce the CSPG deposition that occurred following injury. Results: Early and robust upregulation of CSPGs following lysolecithin-induced demyelination was cleared during remyelination. In culture, CSPGs anchored onto the substratum reduced the adhesion of mouse and human OPCs and their subsequent morphological differentiation into process-bearing oligodendrocytes. Soluble CSPGs added to already adherent OPCs reduced the development of processes, whereas the acquisition of mature myelin proteins was unimpeded. Stripe assays of alternating CSPG and control substrata confirmed the nonpermissive nature of CSPGs for OPC adhesion and morphological differentiation. Enzymatic degradation of CSPGs with chondroitinase ABC was sufficient to overcome CSPG-dependent inhibition of human oligodendrocytes. Finally, in vivo xyloside treatment to reduce CSPG synthesis in lysolecithin-demyelinated mice increased numbers of OPCs and oligodendrocytes in lesions, and culminated in improved remyelination. Interpretation: These results identify CSPGs as a nonpermissive substrate for OPCs and oligodendrocytes, and as a prominent impediment to remyelination. The data suggest the requirement for the neutralization of CSPGs for repair after demyelination. ANN NEUROL 2012;72:419-432. [ABSTRACT FROM AUTHOR]