I21: an advanced high-resolution resonant inelastic X-ray scattering beamline at Diamond Light Source.

The I21 beamline at Diamond Light Source is dedicated to advanced resonant inelastic X-ray scattering (RIXS) for probing charge, orbital, spin and lattice excitations in materials across condensed matter physics, applied sciences and chemistry. Both the beamline and the RIXS spectrometer employ divergent variable-line-spacing gratings covering a broad energy range of 280-3000 eV. A combined energy resolution of ∼35 meV (16 meV) is readily achieved at 930 eV (530 eV) owing to the optimized optics and the mechanics.

I22: SAXS/WAXS beamline at Diamond Light Source - an overview of 10 years operation.

Beamline I22 at Diamond Light Source is dedicated to the study of soft-matter systems from both biological and materials science. The beamline can operate in the range 3.7 keV to 22 keV for transmission SAXS and 14 keV to 20 keV for microfocus SAXS with beam sizes of 240 µm × 60 µm [full width half-maximum (FWHM) horizontal (H) × vertical (V)] at the sample for the main beamline, and approximately 10 µm × 10 µm for the dedicated microfocusing platform.

The NanI and NanJ sialidases of Clostridium perfringens are not essential for virulence.

The essential toxin in Clostridium perfringens-mediated gas gangrene or clostridial myonecrosis is alpha-toxin, although other toxins and extracellular enzymes may also be involved. In many bacterial pathogens extracellular sialidases are important virulence factors, and it has been suggested that sialidases may play a role in gas gangrene. C.

Cross-complementation of Clostridium perfringens PLC and Clostridium septicum alpha-toxin mutants reveals PLC is sufficient to mediate gas gangrene.

Clostridium perfringens and Clostridium septicum are the most common causes of clostridial myonecrosis or gas gangrene. Although they mediate a similar disease pathology, they elaborate functionally very different alpha-toxins. We used a reciprocal complementation approach to assess the contribution of the primary toxin of each species to disease and found that C.

Pore-forming activity of alpha-toxin is essential for clostridium septicum-mediated myonecrosis.

Clostridium septicum alpha-toxin is a beta-barrel pore-forming cytolysin that is functionally similar to aerolysin. Residues important in receptor binding, oligomerization, and pore formation have been identified; however, little is known about the activity of the toxin in an infection, although it is essential for disease. We have now shown that deletion of a small portion of the transmembrane domain, so that the toxin is no longer able to form pores, completely abrogates its ability to contribute to disease, as does replacement of the sole cysteine residue with leucine.

Administration of porcine interleukin-3 induces increased levels of blood eosinophils.

Increasing resistance to anthelmintic drugs indicates a vital need to develop alternative strategies to control helminth infections. Interleukin-3 (IL-3) is a multilineage hematopoietic growth regulator produced by activated T lymphocytes in response to infection. In helminth infections, eosinophils play an important role in the elimination of parasites through their recruitment of inflammatory cells and the release of granules.

Molecular and cellular basis of microvascular perfusion deficits induced by Clostridium perfringens and Clostridium septicum.

Reduced tissue perfusion leading to tissue ischemia is a central component of the pathogenesis of myonecrosis caused by Clostridium perfringens. The C. perfringens alpha-toxin has been shown capable of inducing these changes, but its potential synergy with perfringolysin O (theta-toxin) is less well understood.

The alpha-toxin of Clostridium septicum is essential for virulence.

Clostridium septicum is the causative agent of spontaneous gas gangrene or atraumatic myonecrosis, a sudden and frequently fatal infection that is increasingly associated with malignancy of the colon. Little is known about the disease process although the focus of virulence studies has been the alpha-toxin, a pore-forming cytolysin that is encoded by the csa gene and secreted as an inactive protoxin. Until now a lack of techniques for the genetic manipulation of C.

Serological responses against the pathogenic dimorphic fungus Mucor amphibiorum in populations of platypus (Ornithorhynchus anatinus) with and without ulcerative mycotic dermatitis.

Mucor amphibiorum, a dimorphic fungus, causes ulcerative dermatitis and systemic infections in the platypus Ornithorhynchus anatinus in some river systems in Tasmania but apparently not in other regions of Australia. As yet there are no suitable tests for population surveys, nor for detection of internal lesions in live animals. Consequently, immunoglobulins were purified from the serum of platypuses and anti-immunoglobulin antisera were prepared in rabbits in order to develop an enzyme-linked immunosorbent assay (ELISA) for anti-M.

Synergistic effects of alpha-toxin and perfringolysin O in Clostridium perfringens-mediated gas gangrene.

To examine the synergistic effects of alpha-toxin and perfringolysin O in clostridial myonecrosis, homologous recombination was used to construct an alpha-toxin deficient derivative of a perfringolysin O mutant of Clostridium perfringens. The subsequent strain was complemented with separate plasmids that carried the alpha-toxin structural gene (plc), the perfringolysin O gene (pfoA), or both toxin genes, and the resultant isogenic strains were examined in a mouse myonecrosis model. Synergistic effects were clearly observed in these experiments.

Construction and virulence testing of a collagenase mutant of Clostridium perfringens.

Clostridium perfringens produces several extracellular toxins and enzymes, including an extracellular collagenase or kappa toxin that is encoded by the colA gene. To determine if the ability to produce collagenase was a significant virulence factor in cases of gas gangrene or clostridial myonecrosis that are caused by C. perfringens, a chromosomal colA mutant was constructed by homologous recombination and subsequently virulence tested in the mouse myonecrosis model.

Use of genetically manipulated strains of Clostridium perfringens reveals that both alpha-toxin and theta-toxin are required for vascular leukostasis to occur in experimental gas gangrene.

A hallmark of gas gangrene (clostridial myonecrosis) pathology is a paucity of leukocytes infiltrating the necrotic tissue. The cause of this paucity most likely relates to the observation of leukocyte aggregates at the border of the area of tissue necrosis, often within the microvasculature itself. Infecting mice with genetically manipulated strains of Clostridium perfringens type A (deficient in either alpha-toxin or theta-toxin production) resulted in significantly reduced leukocyte aggregation when alpha-toxin was absent and complete abrogation of leukocyte aggregation when theta-toxin was absent.