New In Situ Method For Measuring Seston Uptake By Suspension-Feeding Bivalve Molluscs

The most commonly used methods for measuring the amount of seston removed from the water column (uptake) by populations of suspension-feeding bivalve molluscs involve taking discrete water samples followed by laboratory analyses. Here we describe a new method based on in situ fluorometry that provides rapid measurement of seston removal rates. The new system is comprised of two identical units, each consisting of an in situ fluorometer, data logger and peristaltic pump with plastic tube attached to a deployment device. The deployment device allows precise placement of the fluorometer probe and intake end of the plastic tube so that in situ fluorescence (chlorophyll a) can be measured and water can be sampled for seston analyses in the laboratory from the same height. The typical setup involves placing one unit upstream and the other downstream of the study area and sampling the water at periodic intervals. Changes in seston concentration are revealed in the field by the fluorometers, and the sampled water can be analyzed in the laboratory for various seston parameters. Comparisons of the in situ data with data from laboratory analyses of pumped water samples were made for three species at four study sites: the eastern oyster (Crassostrea virginica), hard clam (Mercenaria mercenaria), and blue mussel (Mytilus edulis). Comparisons of measured upstream versus downstream seston concentrations indicated significant (t-tests, P \u3c 0.05) differences (uptake) for six of eight trials based on in situ fluorometry, but only marginally significant (P \u3c 0.10) differences at two of the four trials using laboratory chlorophyll a measurements. These data demonstrate that compared with sampling methods requiring laboratory analyses, the new in situ method provides much more rapid quantitative assessments and may provide more accurate estimates

Inequivalent contact structures on Boothby-Wang 5-manifolds

We consider contact structures on simply-connected 5-manifolds which arise as circle bundles over simply-connected symplectic 4-manifolds and show that invariants from contact homology are related to the divisibility of the canonical class of the symplectic structure. As an application we find new examples of inequivalent contact structures in the same equivalence class of almost contact structures with non-zero first Chern class.Comment: 27 pages; to appear in Math. Zeitschrif

Comparison between electrically-evoked and voluntary wrist movements on sensorimotor and prefrontal cortical activation: A multi-channel time domain functional NIRS study

Neuromuscular electrical stimulation (NMES) has been consistently demonstrated to improve skeletal muscle function in neurological populations with movement disorders, such as poststroke and incomplete spinal cord injury (Vanderthommen and Duchateau, 2007). Recent research has documented that rapid, supraspinal central nervous system reorganisation/neuroplastic mechanisms are also implicated during NMES (Chipchase et al., 2011). Functional neuroimaging studies have shown NMES to activate a network of sub-cortical and cortical brain regions, including the sensorimotor (SMC) and prefrontal (PFC) cortex (Blickenstorfer et al., 2009; Han et al., 2003; Muthalib et al., 2012). A relationship between increase in SMC activation with increasing NMES current intensity up to motor threshold has been previously reported using functional MRI (Smith et al., 2003). However, since clinical neurorehabilitation programmes commonly utilise NMES current intensities above the motor threshold and up to the maximum tolerated current intensity (MTI), limited research has determined the cortical correlates of increasing NMES current intensity at or above MTI (Muthalib et al., 2012). In our previous study (Muthalib et al., 2012), we assessed contralateral PFC activation using 1-channel functional near infrared spectroscopy (fNIRS) during NMES of the elbow flexors by increasing current intensity from motor threshold to greater than MTI and showed a linear relationship between NMES current intensity and the level of PFC activation. However, the relationship between NMES current intensity and activation of the motor cortical network, including SMC and PFC, has not been clarified. Moreover, it is of scientific and clinical relevance to know how NMES affects the central nervous system, especially in comparison to voluntary (VOL) muscle activation. Therefore, the aim of this study was to utilise multi-channel time domain fNIRS to compare SMC and PFC activation between VOL and NMESevoked wrist extension movements

Occupationally related bilateral calcific tendonitis of Flexor carpi ulnaris: case report

We present a case of bilateral calcific tendonitis of the Flexor Carpi Ulnaris attributable to repetitive wrist action which was occupationally related. This was treated conservatively with avoidance of aggravating movement, resting splints and anti inflammatory medication when acute flare ups occurred. Since avoidance of repetitive strain on the wrists he has had no further flare ups in over 2 years. This is the only case of bilateral calcific tendonitis of Flexor Carpi Ulnaris that has been reported in the literature, further more it is the only one which has been attributed to occupation and settled following a change of career

Lyman Alpha Blobs as an Observational Signature of Cold Accretion Streams into Galaxies

Recent hydrodynamic simulations of galaxy formation reveal streams of cold (T ~ 1e4 K) gas flowing into the centers of dark matter halos as massive as 1e12-1e13.5 M_sun at redshifts z~1-3. In this paper we show that if > 20% of the gravitational binding energy of the gas is radiated away, then the simulated cold flows are spatially extended Lyman Alpha (Lya) sources with luminosities, Lya line widths, and number densities that are comparable to those of observed Lya blobs. Furthermore, the filamentary structure of the cold flows can explain the wide range of observed Lya blob morphologies. Since the most massive halos form in dense environments, the association of Lya blobs with overdense regions arise naturally. We argue that Lya blobs - even those which are clearly associated with starburst galaxies or quasars - provide direct observational support for the cold accretion mode of galaxies. We discuss various testable predictions of this association.Comment: MNRAS in press. 13 pages, 6 figures. Discussion + references added. Main conclusions unaffecte

A galU mutant of francisella tularensis is attenuated for virulence in a murine pulmonary model of tularemia

<p>Abstract</p> <p>Background</p> <p>A number of studies have revealed that <it>Francisella tularensis </it>(FT) suppresses innate immune responses such as chemokine/cytokine production and neutrophil recruitment in the lungs following pulmonary infection via an unidentified mechanism. The ability of FT to evade early innate immune responses could be a very important virulence mechanism for this highly infectious bacterial pathogen.</p> <p>Results</p> <p>Here we describe the characterization of a <it>galU </it>mutant strain of FT live vaccine strain (LVS). We show that the <it>galU </it>mutant was highly attenuated in a murine model of tularemia and elicited more robust innate immune responses than the wild-type (WT) strain. These studies document that the kinetics of chemokine expression and neutrophil recruitment into the lungs of mice challenged with the <it>galU </it>mutant strain are significantly more rapid than observed with WT FT, despite the fact that there were no observed differences in TLR2 or TLR4 signaling or replication/dissemination kinetics during the early stages of infection. We also show that the <it>galU </it>mutant had a hypercytotoxic phenotype and more rapidly induced the production of IL-1β following infection either <it>in vitro </it>or <it>in vivo</it>, indicating that attenuation of the <it>galU </it>mutant strain may be due (in part) to more rapid activation of the inflammasome and/or earlier death of FT infected cells. Furthermore, we show that infection of mice with the <it>galU </it>mutant strain elicits protective immunity to subsequent challenge with WT FT.</p> <p>Conclusions</p> <p>Disruption of the <it>galU </it>gene of FTLVS has little (if any) effect on <it>in vivo </it>infectivity, replication, or dissemination characteristics, but is highly attenuating for virulence. The attenuated phenotype of this mutant strain of FT appears to be related to its increased ability to induce innate inflammatory responsiveness, resulting in more rapid recruitment of neutrophils to the lungs following pneumonic infection, and/or to its ability to kill infected cells in an accelerated fashion. These results have identified two potentially important virulence mechanisms used by FT. These findings could also have implications for design of a live attenuated vaccine strain of FT because sublethal infection of mice with the <it>galU </it>mutant strain of FTLVS promoted development of protective immunity to WT FTLVS.</p

Oral tolerance to cancer can be abrogated by T regulatory cell inhibition

Oral administration of tumour cells induces an immune hypo-responsiveness known as oral tolerance. We have previously shown that oral tolerance to a cancer is tumour antigen specific, non-cross-reactive and confers a tumour growth advantage. We investigated the utilisation of regulatory T cell (Treg) depletion on oral tolerance to a cancer and its ability to control tumour growth. Balb/C mice were gavage fed homogenised tumour tissue – JBS fibrosarcoma (to induce oral tolerance to a cancer), or PBS as control. Growth of subcutaneous JBS tumours were measured; splenic tissue excised and flow cytometry used to quantify and compare systemic Tregs and T effector (Teff) cell populations. Prior to and/or following tumour feeding, mice were intraperitoneally administered anti-CD25, to inactivate systemic Tregs, or given isotype antibody as a control. Mice which were orally tolerised prior to subcutaneous tumour induction, displayed significantly higher systemic Treg levels (14% vs 6%) and faster tumour growth rates than controls (p<0.05). Complete regression of tumours were only seen after Treg inactivation and occurred in all groups - this was not inhibited by tumour feeding. The cure rates for Treg inactivation were 60% during tolerisation, 75% during tumour growth and 100% during inactivation for both tolerisation and tumour growth. Depletion of Tregs gave rise to an increased number of Teff cells. Treg depletion post-tolerisation and post-tumour induction led to the complete regression of all tumours on tumour bearing mice. Oral administration of tumour tissue, confers a tumour growth advantage and is accompanied by an increase in systemic Treg levels. The administration of anti-CD25 Ab decreased Treg numbers and caused an increase in Teffs. Most notably Treg cell inhibition overcame established oral tolerance with consequent tumor regression, especially relevant to foregut cancers where oral tolerance is likely to be induced by the shedding of tumour tissue into the gut

Mapping spot blotch resistance genes in four barley populations

Bipolaris sorokiniana (teleomorph: Cochliobolus sativus) is the fungal pathogen responsible for spot blotch in barley (Hordeum vulgare L.) and occurs worldwide in warmer, humid growing conditions. Current Australian barley varieties are largely susceptible to this disease and attempts are being made to introduce sources of resistance from North America. In this study we have compared chromosomal locations of spot blotch resistance reactions in four North American two-rowed barley lines; the North Dakota lines ND11231-12 and ND11231-11 and the Canadian lines TR251 and WPG8412-9-2-1. Diversity Arrays Technology (DArT)-based PCR, expressed sequence tag (EST) and SSR markers have been mapped across four populations derived from crosses between susceptible parental lines and these four resistant parents to determine the location of resistance loci. Quantitative trait loci (QTL) conferring resistance to spot blotch in adult plants (APR) were detected on chromosomes 3HS and 7HS. In contrast, seedling resistance (SLR) was controlled solely by a locus on chromosome 7HS. The phenotypic variance explained by the APR QTL on 3HS was between 16 and 25% and the phenotypic variance explained by the 7HS APR QTL was between 8 and 42% across the four populations. The SLR QTL on 7HS explained between 52 to 64% of the phenotypic variance. An examination of the pedigrees of these resistance sources supports the common identity of resistance in these lines and indicates that only a limited number of major resistance loci are available in current two-rowed germplasm

Combined Inflammatory and Metabolic Defects Reflected by Reduced Serum Protein Levels in Patients with Buruli Ulcer Disease

Buruli ulcer is a skin disease caused by Mycobacterium ulcerans that is spreading in tropical countries, with major public health and economic implications in West Africa. Multi-analyte profiling of serum proteins in patients and endemic controls revealed that Buruli ulcer disease down-regulates the circulating levels of a large array of inflammatory mediators, without impacting on the leukocyte composition of peripheral blood. Notably, several proteins contributing to acute phase reaction, lipid metabolism, coagulation and tissue remodelling were also impacted. Their down-regulation was selective and persisted after the elimination of bacteria with antibiotic therapy. It involved proteins with various functions and origins, suggesting that M. ulcerans infection causes global and chronic defects in the host’s protein metabolism. Accordingly, patients had reduced levels of total serum proteins and blood urea, in the absence of signs of malnutrition, or functional failure of liver or kidney. Interestingly, slow healers had deeper metabolic and coagulation defects at the start of antibiotic therapy. In addition to providing novel insight into Buruli ulcer pathogenesis, our study therefore identifies a unique proteomic signature for this disease

Feedback control architecture and the bacterial chemotaxis network.

PMCID: PMC3088647This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.Bacteria move towards favourable and away from toxic environments by changing their swimming pattern. This response is regulated by the chemotaxis signalling pathway, which has an important feature: it uses feedback to 'reset' (adapt) the bacterial sensing ability, which allows the bacteria to sense a range of background environmental changes. The role of this feedback has been studied extensively in the simple chemotaxis pathway of Escherichia coli. However it has been recently found that the majority of bacteria have multiple chemotaxis homologues of the E. coli proteins, resulting in more complex pathways. In this paper we investigate the configuration and role of feedback in Rhodobacter sphaeroides, a bacterium containing multiple homologues of the chemotaxis proteins found in E. coli. Multiple proteins could produce different possible feedback configurations, each having different chemotactic performance qualities and levels of robustness to variations and uncertainties in biological parameters and to intracellular noise. We develop four models corresponding to different feedback configurations. Using a series of carefully designed experiments we discriminate between these models and invalidate three of them. When these models are examined in terms of robustness to noise and parametric uncertainties, we find that the non-invalidated model is superior to the others. Moreover, it has a 'cascade control' feedback architecture which is used extensively in engineering to improve system performance, including robustness. Given that the majority of bacteria are known to have multiple chemotaxis pathways, in this paper we show that some feedback architectures allow them to have better performance than others. In particular, cascade control may be an important feature in achieving robust functionality in more complex signalling pathways and in improving their performance