Wigner transform and pseudodifferential operators on symmetric spaces of non-compact type

We obtain a general expression for a Wigner transform (Wigner function) on symmetric spaces of non-compact type and study the Weyl calculus of pseudodifferential operators on them

Automatic Analysis of Composite Physical Signals Using Non-Negative Factorization and Information Criterion

In time-resolved spectroscopy, composite signal sequences representing energy transfer in fluorescence materials are measured, and the physical characteristics of the materials are analyzed. Each signal sequence is represented by a sum of non-negative signal components, which are expressed by model functions. For analyzing the physical characteristics of a measured signal sequence, the parameters of the model functions are estimated. Furthermore, in order to quantitatively analyze real measurement data and to reduce the risk of improper decisions, it is necessary to obtain the statistical characteristics from several sequences rather than just a single sequence. In the present paper, we propose an automatic method by which to analyze composite signals using non-negative factorization and an information criterion. The proposed method decomposes the composite signal sequences using non-negative factorization subjected to parametric base functions. The number of components (i.e., rank) is also estimated using Akaike's information criterion. Experiments using simulated and real data reveal that the proposed method automatically estimates the acceptable ranks and parameters

Nanoimprinting of biomedical polymers reduces candidal physical adhesion

Management of fungal biofilms represents a significant challenge to healthcare. As a preventive approach, minimising adhesion between indwelling medical devices and microorganisms would be an important step forward. This study investigated the anti-fouling capacity of engineered nanoscale topographies to the pathogenic yeast Candida albicans. Highly ordered arrays of nano-pit topographies were shown to significantly reduce the physical adherence capacity of C. albicans. This study shows a potential of nanoscale patterns to inhibit and prevent pathogenic biofilm formation on biomedical substrates

Neuronal characteristics of small-cell lung cancer

Wide ranging experimental evidence suggests that human small-cell lung cancer (SCLC) has a number of molecular and subcellular characteristics normally associated with neurones. This review outlines and discusses these characteristics in the light of recent developments in the field. Emphasis is placed upon neuronal cell adhesion molecules, neurone-restrictive silencer factor, neurotransmitters/peptides and voltage-gated ion, especially Na+ channels. The hypothesis is put forward that acquisition of such characteristics and the membrane ‘excitability' that would follow can accelerate metastatic progression. The clinical potential of the neuronal characteristics of SCLC, in particular ion channel expression/activity, is discussed in relation to possible novel diagnostic and therapeutic modalities

Sophorolipid biosurfactants: Possible uses as antibacterial and antibiofilm agent.

Biosurfactants are amphipathic, surface-active molecules of microbial origin which accumulate at interfaces reducing interfacial tension and leading to the formation of aggregated micellular structures in solution. Some biosurfactants have been reported to have antimicrobial properties, the ability to prevent adhesion and to disrupt biofilm formation. We investigated antimicrobial properties and biofilm disruption using sophorolipids at different concentrations. Growth of Gram negative Cupriavidus necator ATCC 17699 and Gram positive Bacillus subtilis BBK006 were inhibited by sophorolipids at concentrations of 5% v/v with a bactericidal effect. Sophorolipids (5% v/v) were also able to disrupt biofilms formed by single and mixed cultures of B. subtilis BBK006 and Staphylococcus aureus ATCC 9144 under static and flow conditions, as was observed by scanning electron microscopy. The results indicated that sophorolipids may be promising compounds for use in biomedical application as adjuvants to other antimicrobial against some pathogens through inhibition of growth and/or biofilm disruption

Transmission electron microscopy characterization of fluorescently labelled amyloid β 1-40 and α-synuclein aggregates

<p>Abstract</p> <p>Background</p> <p>Fluorescent tags, including small organic molecules and fluorescent proteins, enable the localization of protein molecules in biomedical research experiments. However, the use of these labels may interfere with the formation of larger-scale protein structures such as amyloid aggregates. Therefore, we investigate the effects of some commonly used fluorescent tags on the morphologies of fibrils grown from the Alzheimer's disease-associated peptide Amyloid β 1-40 (Aβ40) and the Parkinson's disease-associated protein α-synuclein (αS).</p> <p>Results</p> <p>Using transmission electron microscopy (TEM), we verify that N-terminal labeling of Aβ40 with AMCA, TAMRA, and Hilyte-Fluor 488 tags does not prevent the formation of protofibrils and amyloid fibrils of various widths. We also measure the two-photon action cross-section of Aβ40 labelled with Hilyte Fluor 488 and demonstrate that this tag is suitable for use with two-photon fluorescence techniques. Similarly, we find that Alexa Fluor 488 labelling of αS variant proteins near either the N or C terminus (position 9 or 130) does not interfere with the formation of amyloid and other types of αS fibrils. We also present TEM images of fibrils grown from αS C-terminally labelled with enhanced green fluorescent protein (EGFP). Near neutral pH, two types of αS-EGFP fibrils are observed via TEM, while denaturation of the EGFP tag leads to the formation of additional species.</p> <p>Conclusions</p> <p>We demonstrate that several small extrinsic fluorescent tags are compatible with studies of amyloid protein aggregation. However, although fibrils can be grown from αS labelled with EGFP, the conformation of the fluorescent protein tag affects the observed aggregate morphologies. Thus, our results should assist researchers with label selection and optimization of solution conditions for aggregation studies involving fluorescence techniques.</p

Enhanced biodegradation of PAHs in historically contaminated soil by M. gilvum inoculated biochar

The inoculation of rice straw biochar with PAH-degrading Mycobacterium gilvum (1.27 × 1011 ± 1.24 × 1010 cell g−1), and the subsequent amendment of this composite material to PAHs contaminated (677 mg kg−1) coke plant soil, was conducted in order to investigate if would enhance PAHs biodegradation in soils. The microbe-biochar composite showed superior degradation capacity for phenanthrene, fluoranthene and pyrene. Phenanthrene loss in the microbe-biochar composite, free cell alone and biochar alone treatments was, respectively, 62.6 ± 3.2%, 47.3 ± 4.1% and non-significant (P > 0.05); whereas for fluoranthene loss it was 52.1 ± 2.3%; non-significant (P > 0.05) and non-significant (P > 0.05); and for pyrene loss it was 62.1 ± 0.9%; 19.7 ± 6.5% and 13.5 ± 2.8%. It was hypothesized that the improved remediation was underpinned by i) biochar enhanced mass transfer of PAHs from the soil to the carbonaceous biochar “sink”, and ii) the subsequent degradation of the PAHs by the immobilized M. gilvum. To test this mechanism, a surfactant (Brij 30; 20 mg g−1 soil), was added to impede PAHs mass transfer to biochar and sorption. The surfactant increased solution phase PAH concentrations and significantly (P < 0.05) reduced PAH degradation in the biochar immobilized M. gilvum treatments; indicating the enhanced degradation occurred between the immobilized M. gilvum and biochar sorbed PAHs

Thrombin Induces Macrophage Migration Inhibitory Factor Release and Upregulation in Urothelium: A Possible Contribution to Bladder Inflammation

Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine expressed by urothelial cells that mediates bladder inflammation. We investigated the effect of stimulation with thrombin, a Protease Activated Receptor-1 (PAR1) agonist, on MIF release and MIF mRNA upregulation in urothelial cells.MIF and PAR1 expression was examined in normal human immortalized urothelial cells (UROtsa) using real-time RT-PCR, Western blotting and dual immunostaining. MIF and PAR1 immunostaining was also examined in rat urothelium. The effect of thrombin stimulation (100 nM) on urothelial MIF release was examined in UROtsa cells (in vitro) and in rats (in vivo). UROtsa cells were stimulated with thrombin, culture media were collected at different time points and MIF amounts were determined by ELISA. Pentobarbital anesthetized rats received intravesical saline (control), thrombin, or thrombin +2% lidocaine (to block nerve activity) for 1 hr, intraluminal fluid was collected and MIF amounts determined by ELISA. Bladder or UROtsa MIF mRNA was measured using real time RT-PCR.UROtsa cells constitutively express MIF and PAR1 and immunostaining for both was observed in these cells and in the basal and intermediate layers of rat urothelium. Thrombin stimulation of urothelial cells resulted in a concentration- and time-dependent increase in MIF release both in vitro (UROtsa; 2.8-fold increase at 1 hr) and in vivo (rat; 4.5-fold) while heat-inactivated thrombin had no effect. In rats, thrombin-induced MIF release was reduced but not abolished by intravesical lidocaine treatment. Thrombin also upregulated MIF mRNA in UROtsa cells (3.3-fold increase) and in the rat bladder (2-fold increase) where the effect was reduced (1.4-fold) by lidocaine treatment.Urothelial cells express both MIF and PAR1. Activation of urothelial PAR1 receptors, either by locally generated thrombin or proteases present in the urine, may mediate bladder inflammation by inducing urothelial MIF release and upregulating urothelial MIF expression