Quercus suber infected by Phytophthora cinnamomi: effects at cellular level of cinnamomin on roots, stem and leaves

Phytophthora cinnamomi has been reported to be regularly associated with cork and holm oak decline. This oomycete secretes elicitins, a group of unique highly conserved pr oteins that can enhance plant defence reactions

Exposition of cork oak roots to cryptogein reduced the Infection by Phytophtora cinnamomi

The oomycete P. cinnamomi has been described as strong contributing factor to the decline of cork oak and holm oak stands occurring in the Iberian Peninsula. There are no eradication methods available against this pathogen

Alpha cinnamomin elicits a defence response against Phytophthora cinnamomi in Castanea sativa

Phytophthora cinnamomi and P. cambivora are considered as the causal agents of Castanea sativa ink disease. These soil-borne plant pathogens invade and destroy the root system leading to the death of the trees. Most Phytophthora species secrete elicitins, a group of unique highly conserved proteins that are able to enhance plant defence responses in a systemic acquired resistance manner against infection by several pathogens. A cluster of four elicitin genes was identified in P. cinnamomi. In previous works one of these elicitins, α- cinnamomin was shown to restrict the invasion of root cortical tissues by P. cinnamomi preventing vascular colonization in cork and holm oak. In the present work, roots of chestnut plantlets grown in vitro were allowed to absorb α-cinnamomin at 100 μg/ml for two days before being inoculated with P. cinnamomi. The effects of this elicitin on host-pathogen interaction were studied at histological and ultrastructural levels. P. cinnamomi was restricted to the outer cortex of 65% of the roots pre-treated with α-cinnamomin. In these roots, the vascular cylinders were free of pathogen. On the contrary, the pathogen reached the vascular cylinder, penetrating the phloem and xylem vessels in all non-treated assayed roots. The signs of pathogen degradation in the cortical parenchyma, mainly in the intercellular spaces, and the increase of a physical barrier in epidermal and sub-epidermal cell wall-media lamella and intercellular spaces by impregnation with phenol-like compounds strongly suggest that α-cinnamomin induced in chestnut defence reactions against P. cinnamomi

Scapular dynamic muscular stiffness assessed through myotonometry: a narrative review

Several tools have been used to assess muscular stiffness. Myotonometry stands out as an accessible, handheld, and easy to use tool. The purpose of this review was to summarize the psychometric properties and methodological considerations of myotonometry and its applicability in assessing scapular muscles. Myotonometry seems to be a reliable method to assess several muscles stiffness, as trapezius. This method has been demonstrated fair to moderate correlation with passive stiffness measured by shear wave elastography for several muscles, as well as with level of muscle contraction, pinch and muscle strength, Action Research Arm Test score and muscle or subcutaneous thickness. Myotonometry can detect scapular muscles stiffness differences between pre- and post-intervention in painful conditions and, sometimes, between symptomatic and asymptomatic subjects.info:eu-repo/semantics/publishedVersio

A utilização de elicitinas no combate contra Phytophthora cinnamomi na doença da tinta do castanheiro e no declínio do montado

Phytophthora cinnamomi e P. cambivora são considerados os agentes patogénicos da doença da tinta do castanheiro. Estes agentes invadem e destroem o sistema radicular, levando à morte das árvores e a importantes perdas económicas. O declínio do montado tem sido associado a vários agentes patogénicos, pragas e factores abióticos. Phytophthora cinnamomi tem sido referido como um potencial agente patogénico do sobreiro e azinheira. O aparecimento de mais estirpes de microrganismos patogénicos resistentes a pesticidas impõe o desenvolvimento de novas estratégias de biocontrolo, entre as quais a estimulação de reações de defesa. As elicitinas são proteínas de baixo peso molecular, secretadas por algumas espécies de oomycetes (Phytophthora e Pythium) que induzem reações de hipersensibilidade e aquisição de resistência sistémica nas plantas, contra um grande número de bactérias e fungos patogénicos. Este trabalho é uma síntese dos resultados sobre o efeito da aplicação radicular de várias elicitinas, na infeção do sobreiro, azinheira e castanheiro por P. cinnamomi. A avaliação foi efetuada por observação microscópica dos tecidos invadidos, em especial dos tecidos vasculares. Observou‑se a indução de reações de defesa contra P. cinnamomi quando se submeteram as raízes destas três espécies a pré‑tratamento com as elicitinas criptogeína, capsiceína ou cinamomina. A infeção ficou restrita aos tecidos corticais da raiz, onde o agente patogénico se desorganizou e não progrediu para os vasos, estando associado à acumulação de materiais que se presume serem tóxicos, produzidos nas células dos hospedeiros, em contato com as hifas em desorganização. Os ensaios laboratoriais indicaram que as elicitinas testadas se revelaram muito eficientes no biocontrolo de P. cinnamomi. Será de grande importância desenvolver tecnologia no sentido de obtenção de elicitinas a baixo custo e de criar sistemas eficientes da sua dispersão nas plantas

Exciting flavored bound states

We study ground and radial excitations of flavor singlet and flavored pseudoscalar mesons within the framework of the rainbow-ladder truncation using an infrared massive and finite interaction in agreement with recent results for the gluon-dressing function from lattice QCD and Dyson-Schwinger equations. Whereas the ground-state masses and decay constants of the light mesons as well as charmonia are well described, we confirm previous observations that this truncation is inadequate to provide realistic predictions for the spectrum of excited and exotic states. Moreover, we find a complex conjugate pair of eigenvalues for the excited $D_{(s)}$ mesons, which indicates a non-Hermiticity of the interaction kernel in the case of heavy-light systems and the present truncation. Nevertheless, limiting ourselves to the leading contributions of the Bethe-Salpeter amplitudes, we find a reasonable description of the charmed ground states and their respective decay constants.Comment: 10 pages, 1 figure, 3 tables; various typos corrected; 3 additional references; as published in PR

Lifetime imaging of a fluorescent protein sensor reveals surprising stability of ER thiol redox.

Interfering with disulfide bond formation impedes protein folding and promotes endoplasmic reticulum (ER) stress. Due to limitations in measurement techniques, the relationships of altered thiol redox and ER stress have been difficult to assess. We report that fluorescent lifetime measurements circumvented the crippling dimness of an ER-tuned fluorescent redox-responsive probe (roGFPiE), faithfully tracking the activity of the major ER-localized protein disulfide isomerase, PDI. In vivo lifetime imaging by time-correlated single-photon counting (TCSPC) recorded subtle changes in ER redox poise induced by exposure of mammalian cells to a reducing environment but revealed an unanticipated stability of redox to fluctuations in unfolded protein load. By contrast, TCSPC of roGFPiE uncovered a hitherto unsuspected reductive shift in the mammalian ER upon loss of luminal calcium, whether induced by pharmacological inhibition of calcium reuptake into the ER or by physiological activation of release channels. These findings recommend fluorescent lifetime imaging as a sensitive method to track ER redox homeostasis in mammalian cells

Unfolding kinetics of beta-lactoglobulin induced by surfactant and denaturant: a stopped-flow/fluorescence study

The beta ->alpha transition of beta-lactoglobulin, a globular protein abundant in the milk of several mammals, is investigated in this work. This transition, induced by the cationic surfactant dodecyltrimethylammonium chloride (DTAC), is accompanied by partial unfolding of the protein. In this work, unfolding of bovine beta-lactoglobulin in DTAC is compared with its unfolding induced by the chemical denaturant guanidine hydrochloride (GnHCl). The final protein states attained in the two media have quite different secondary structure: in DTAC the alpha-helical content increases, leading to the so-called alpha-state; in GnHCl the amount of ordered secondary-structure decreases, resulting in a random coil-rich final state (denatured, or D, state). To obtain information on both mechanistic routes, in DTAC and GnHCl, and to characterize intermediates, the kinetics of unfolding were investigated in the two media. Equilibrium and kinetic data show the partial accumulation of an on-pathway intermediate in each unfolding route: in DTAC, an intermediate (I-1) with mostly native secondary structure but loose tertiary structure appears between the native (beta) and alpha-states; in GnHCl, another intermediate (I-2) appears between states beta and D. Kinetic rate constants follow a linear Chevron-plot representation in GnHCl, but show a more complex mechanism in DTAC, which acts like a stronger binding species.info:eu-repo/semantics/publishedVersio

Effects of ventilation strategy on distribution of lung inflammatory cell activity

Introduction: Leukocyte infiltration is central to the development of acute lung injury, but it is not known how mechanical ventilation strategy alters the distribution or activation of inflammatory cells. We explored how protective (vs. injurious) ventilation alters the magnitude and distribution of lung leukocyte activation following systemic endotoxin administration. Methods: Anesthetized sheep received intravenous endotoxin (10 ng/kg/min) followed by 2 h of either injurious or protective mechanical ventilation (n = 6 per group). We used positron emission tomography to obtain images of regional perfusion and shunting with infused 13N[nitrogen]-saline and images of neutrophilic inflammation with 18F-fluorodeoxyglucose (18F-FDG). The Sokoloff model was used to quantify 18F-FDG uptake (Ki), as well as its components: the phosphorylation rate (k3, a surrogate of hexokinase activity) and the distribution volume of 18F-FDG (Fe) as a fraction of lung volume (Ki = Fe × k3). Regional gas fractions (fgas) were assessed by examining transmission scans. Results: Before endotoxin administration, protective (vs. injurious) ventilation was associated with a higher ratio of partial pressure of oxygen in arterial blood to fraction of inspired oxygen (PaO2/FiO2) (351 ± 117 vs. 255 ± 74 mmHg; P < 0.01) and higher whole-lung fgas (0.71 ± 0.12 vs. 0.48 ± 0.08; P = 0.004), as well as, in dependent regions, lower shunt fractions. Following 2 h of endotoxemia, PaO2/FiO2 ratios decreased in both groups, but more so with injurious ventilation, which also increased the shunt fraction in dependent lung. Protective ventilation resulted in less nonaerated lung (20-fold; P < 0.01) and more normally aerated lung (14-fold; P < 0.01). Ki was lower during protective (vs. injurious) ventilation, especially in dependent lung regions (0.0075 ± 0.0043/min vs. 0.0157 ± 0.0072/min; P < 0.01). 18F-FDG phosphorylation rate (k3) was twofold higher with injurious ventilation and accounted for most of the between-group difference in Ki. Dependent regions of the protective ventilation group exhibited lower k3 values per neutrophil than those in the injurious ventilation group (P = 0.01). In contrast, Fe was not affected by ventilation strategy (P = 0.52). Lung neutrophil counts were not different between groups, even when regional inflation was accounted for. Conclusions: During systemic endotoxemia, protective ventilation may reduce the magnitude and heterogeneity of pulmonary inflammatory cell metabolic activity in early lung injury and may improve gas exchange through its effects predominantly in dependent lung regions. Such effects are likely related to a reduction in the metabolic activity, but not in the number, of lung-infiltrating neutrophils