OxyEMG: an application for determination of the oxyspinel group end-members based on electron microprobe analyses

The Oxyspinel group End-Member Generator (OxyEMG) is an improved version of the EMG application. This new version allows for calculating, based on electron microprobe analysis (EMPA), the proportions of 31 end-member components in an oxyspinel composition. These components are MgAl2O4 (spinel), FeAl2O4 (hercynite), MnAl2O4 (galaxite), ZnAl2O4 (gahnite), NiAl2O4 (chihmingite), CuAl2O4 (thermaerogenite), MgFe2O4 (magnesioferrite), Fe3O4 (magnetite), MnFe2O4 (jacobsite), ZnFe2O4 (franklinite), NiFe2O4 (trevorite), CuFe2O4 (cuprospinel), FeMn2O4, MgMn2O4, Mn3O4 (hausmannite), ZnMn2O4 (hetaerolite), MgCr2O4 (magnesiochromite), FeCr2O4 (chromite), MnCr2O4 (manganochromite), ZnCr2O4 (zincochromite), NiCr2O4 (nichromite), CoCr2O4 (cochromite), MgV2O4 (magnesiocoulsonite), FeV2O4 (coulsonite), MnV2O4 (vuorelainenite), Co3O4 (guite), TiMg2O4 (qandilite), TiFe2O4 (ulvöspinel), SiMg2O4 (ringwoodite), SiFe2O4 (ahrensite) and GeFe2O4 (brunogeierite). Compared with the older version, OxyEMG allows for (a) calculating 12 additional oxyspinel group end-member compositions (chihmingite, thermaerogenite, hausmannite, hetaerolite, FeMn2O4, MgMn2O4, cuprospinel, cochromite, guite, ringwoodite, ahrensite and brunogeierite), (b) discriminating the cation valency not only for Fe2+–Fe3+ but also for Mn2+–Mn3+ and Co2+–Co3+, and (c) changing the method to calculate the components of the magnetite and ulvöspinel prisms. As in EMG, this new version is an application that does not require an installation process and was created with the purpose of performing calculations to obtain cation proportions (per formula unit, p.f.u.), end-members of the oxyspinel group, a ΣR3+ value, a ΣR2+ value, ΣR3+ / ΣR2+ ratios, redistribution proportions for the corresponding end-members in the magnetite or ulvöspinel prisms, and a data validation section to check the results.</p

Contracaecumovale (Nematoda: Anisakidae) from Rollandia rolland Quoy & Gaimard 1824 (Aves, Podicipedidae) in Argentina Contracaecumovale (Nematoda: Anisakidae) de Rollandia rolland Quoy & Gaimard 1824 (Aves, Podicipedidae) na Argentina

Necropsy on 15 specimens of white-tufted grebe, Rollandiarolland, caught in the Mar Chiquita and Chascomús lagoons (Buenos Aires province), revealed the presence of Contracaecumovale (Linstow, 1907). This nematode shows a marked specificity for podicipediform birds. The specimens were identified from morphological study on features such as cephalic and esophageal structures and caudal papillae, using both optical and scanning electron microscopy. This is the first record of C. ovale parasitizing R. rolland in Argentina.<br>Necropsia de 15 espécimes de mergulhão-de-orelha-branca, Rollandiarolland, coletados nas lagoas Mar Chiquita e Chascomús (Província de Buenos Aires), revelou a presença de Contracaecumovale (Linstow, 1907). Esse nematóide tem uma marcada especificidade pelas aves podicipediformes. Os espécimes foram identificados a partir de características, tais como estruturas morfológicas cefálicas e esofágicas e papilas caudais, utilizando-se microscopia óptica e microscopia eletrônica de varredura (MEV). Esse é o primeiro registro de C. ovale parasito de R. rolland na Argentina

The naïve airway hyperresponsiveness of the A/J mouse is Kit-mediated

There is a wide variation among humans and mice in airway hyperresponsiveness (AHR) in the absence of allergen sensitization, i.e., naïve AHR. Because mast cell (MC) activation is thought to mediate AHR in atopic asthmatic subjects, we asked whether MCs mediate naïve AHR in A/J mice. We generated an A/J congenic strain lacking c-Kit by introgression of the Wv mutation, which resulted in the elimination of MCs and the abrogation of naïve AHR. Imatinib, which disrupts Kit signaling, also abrogated AHR in A/J mice. Remarkably, introduction of the Vga9 Mitf mutation into the A/J background resulted in the ablation of MCs but did not ameliorate AHR. These results indicate that c-Kit is required for development of AHR in an MC-independent fashion

Glia and Mast Cells as Targets for Palmitoylethanolamide, an Anti-inflammatory and Neuroprotective Lipid Mediator

Glia are key players in a number of nervous system disorders. Besides releasing glial and neuronal signaling molecules directed to cellular homeostasis, glia respond also to pro-inflammatory signals released from immune-related cells, with the mast cell being of particular interest. A proposed mast cell-glia communication may open new perspectives for designing therapies to target neuroinflammation by differentially modulating activation of non-neuronal cells normally controlling neuronal sensitization-both peripherally and centrally. Mast cells and glia possess endogenous homeostatic mechanisms/molecules that can be upregulated as a result of tissue damage or stimulation of inflammatory responses. Such molecules include the N-acylethanolamines, whose principal family members are the endocannabinoid N-arachidonoylethanolamine (anandamide), and its congeners N-stearoylethanolamine, N-oleoylethanolamine, and N-palmitoylethanolamine (PEA). A key role of PEA may be to maintain cellular homeostasis when faced with external stressors provoking, for example, inflammation: PEA is produced and hydrolyzed by microglia, it downmodulates mast cell activation, it increases in glutamate-treated neocortical neurons ex vivo and in injured cortex, and PEA levels increase in the spinal cord of mice with chronic relapsing experimental allergic encephalomyelitis. Applied exogenously, PEA has proven efficacious in mast cell-mediated experimental models of acute and neurogenic inflammation. This fatty acid amide possesses also neuroprotective effects, for example, in a model of spinal cord trauma, in a delayed post-glutamate paradigm of excitotoxic death, and against amyloid β-peptide-induced learning and memory impairment in mice. These actions may be mediated by PEA acting through "receptor pleiotropism," i.e., both direct and indirect interactions of PEA with different receptor targets, e.g., cannabinoid CB2 and peroxisome proliferator-activated receptor-alpha