Cytological mechanisms of the development of mucosal candidiasis after exposure to a steroid aerosol preparation

Mucosal candidosis was induced in CBA mice by intraoral inoculation following treatment with corticosteroid-containing aerosol (beclomethasone dipropionate). Histologically, in hormone treated mice the adherence of the pathogen to the mucosal surface was found during the first hours after inoculation. This is followed by the formation of the germ tubes and invasion in the epithelial layer. Pseudomycelial invasion in the malpighian layer is accompanied by the leukocyte response that limits the further spread of the fungal cells. In intact mice, the inoculation is not followed by the effective attachment of the fungal cells to the mucosal surface and induction of mycotic lesions. In vitro experiments have demonstrated the enhanced adherence of fungal blastospores to the epithelial cells of the hormone treated animals, that appears to be one of the mechanisms in the pathogenesis of candidosis in these animals.     

Active transport of amino acids in Thiobacillus thioparus is a low-affinity process.

A method for the isolation of amino acid auxotrophs of Thiobacillus thioparus is described. Characterization of a leucine auxotroph indicated that leucine biosynthesis in T. thioparus was not different from that of heterotrophic bacteria. T. thioparus cells accumulated amino acids via an active mechanism. Kt values of amino acid transport were between 15 and 330 microM, and Vmax values were 200 to 350 pmol min-1 mg of protein-1. Amino acid transport was carried out by a limited number of systems, each responsible for the uptake of several amino acids. Amino acid auxotrophs of T. thioparus exhibited transport and growth properties similar to those of transport-deficient mutants of heterotrophs which lost the high-affinity, but retained the low-affinity, amino acid transport systems.     

The Stress Hormone Corticosterone Increases Synaptic ��-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid (AMPA) Receptors via Serum- and Glucocorticoid-inducible Kinase (SGK) Regulation of the GDI-Rab4 Complex

Corticosterone, the major stress hormone, plays an important role in regulating neuronal functions of the limbic system, although the cellular targets and molecular mechanisms of corticosteroid signaling are largely unknown. Here we show that a short treatment of corticosterone significantly increases α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)-mediated synaptic transmission and AMPAR membrane trafficking in pyramidal neurons of prefrontal cortex, a key region involved in cognition and emotion. This enhancing effect of corticosterone is through a mechanism dependent on Rab4, the small GTPase-controlling receptor recycling between early endosome and plasma membrane. Guanosine nucleotide dissociation inhibitor (GDI), which regulates the cycle of Rab proteins between membrane and cytosol, forms an increased complex with Rab4 after corticosterone treatment. Corticosterone also triggers an increased GDI phosphorylation at Ser-213 by the serum- and glucocorticoid-inducible kinase (SGK). Moreover, AMPAR synaptic currents and surface expression and their regulation by corticosterone are altered by mutating Ser-213 on GDI. These results suggest that corticosterone, via SGK phosphorylation of GDI at Ser-213, increases the formation of GDI-Rab4 complex, facilitating the functional cycle of Rab4 and Rab4-mediated recycling of AMPARs to the synaptic membrane. It provides a potential mechanism underlying the role of corticosteroid stress hormone in up-regulating excitatory synaptic efficacy in cortical neurons.     

Resistivity of Red Blood Cells Against High-Intensity, Short-Duration Electric Field Pulses Induced by Chelating Agents

The interaction of human red blood cells (RBCs) with diethylenetriamine-pentaacetic acid (DTPA) or its Gd-complex (Magnevist, a widely used clinical magnetic resonance contrast agent containing free DTPA ligands) led to the following, obviously interrelated phenomena. (i) Both compounds protected erythrocytes against electrohemolysis in isotonic solutions caused by a high-intensity DC electric field pulse. (ii) The inhibition of electrohemolysis was observed only when cells were electropulsed in low-conductivity solutions. (iii) The uptake of Gd-DTPA by electropulsed RBCs was relatively low. (iv) (Gd-) DTPA reduced markedly deformability of erythrocytes, as revealed by the electrodeformation experiments using high-frequency electric fields. Taken together, the results indicate that (Gd-) DTPA produce stiffer erythrocytes that are more resistant to electric field exposure. The observed effects of the chelating agents on the mechanical properties and the electropermeabilization of RBCs must have an origin in molecular changes of the bilayer or membrane-coupled cytoskeleton, which, in turn, appear to result from an alteration of the ionic equilibrium (e.g., Ca²⁺ sequestration) in the vicinity of the cell membrane. Received: 19 January 1999/Revised: 1 April 1999     

Spontaneous cytotoxicity mediated by invertebrate mononuclear cells toward normal and malignant vertebrate targets: Inhibition by defined mono- and disaccharides

Spontaneous non-antigen-dependent cytotoxicity is displayed in vitro by mononuclear cells from molluscs, annelids, and echinoderms. The cytotoxic potential of these cells appears to be independent of prior antigenic exposure, is easily demonstrated in vitro, and is temperature dependent. The specificity of these cells may be directed at cell-surface glycoproteins on the target cell surface since a variety of defined mono- and disaccharides can block killing. The ability of sugars to block is target cell and effector cell specific. This finding is exactly analogous to our previous finding that human spontaneous monocyte-mediated cytotoxicity is blocked in a target-specific fashion by different mono- and disaccharides. These data suggest that invertebrate as well as vertebrate mononuclear cells may “recognize” targets through a series of sugar-specific “lectin-like” molecules present on the effector cell surface.     

Effect of Phosphate on the Corrosion of Carbon Steel and on the Composition of Corrosion Products in Two-Stage Continuous Cultures of Desulfovibrio desulfuricans

A field isolate of Desulfovibrio desulfuricans was grown in defined medium in a two-stage continuous culture apparatus with different concentrations of phosphate in the feed medium. The first state (V1) was operated as a conventional chemostat (D = 0.045 h⁻¹) that was limited in energy source (lactate) or phosphate. The second stage (V2) received effluent from V1 but no additional nutrients, and contained a healthy population of transiently starved or resting cells. An increase in the concentration of phosphate in the medium fed to V1 resulted in increased corrosion rates of carbon steel in both V1 and V2. Despite the more rapid corrosion observed in growing cultures relative to that in resting cultures, corrosion products that were isolated under strictly anaerobic conditions from the two culture modes had similar bulk compositions which varied with the phosphate content of the medium. Crystalline mackinawite (Fe₉S₈), vivianite [Fe₃(PO₄)₂ · 8H₂O], and goethite [FeO(OH)] were detected in amounts which varied with the culture conditions. Chemical analyses indicated that the S in the corrosion product was almost exclusively in the form of sulfides, while the P was present both as phosphate and as unidentified components, possibly reduced P species. Some differential localization of S and P was observed in intact corrosion products. Cells from lactate-limited, but not from phosphate-limited, cultures contained intracellular granules that were enriched in P and Fe. The results are discussed in terms of several proposed mechanisms of microbiologically influenced corrosion.