Capnodis tenebrionis (Linnaeus, 1758) larval and nymphal lodges dispositions according to physico-chimical composition of Prunus domestica and Prunus cerasus

Capnodis tenebrionis is a Coleoptera presented as a xylophagous insect specialist, common of the Rosaceae orchards. The physico-chemical quality of host plants can provide useful information to define the most appropriate time for control of this pest. From this perspective, the present study focused on the positions of larval lodges of C. tenebrionis on its hosts Prunus spp. The results showed that the larval availability depend on water soluble and soluble proteins in spite of the total sugars on Prunus domestica and of proline on P. cerasus, respectively. The high density of P. cerasus wood appears to have favored the trophic orientation of Capnodis larvae to P. domestica. Therefore, understanding the life history traits of C. tenebrionis will be necessary to improve its monitoring that appears to be influenced by biotic factors.Keywords: Capnodis tenebrionis, Phytochemistry, Physical quality, Rosaceae with nucleus, Variet

Application of a wavelet neural network approach to detect stator winding short circuits in asynchronous machines

Introduction. Nowadays, fault diagnosis of induction machines plays an important role in industrial fields. In this paper, Artificial Neural Network (ANN) model has been proposed for automatic fault diagnosis of an induction machine. The aim of this research study is to design a neural network model that allows generating a large database. This database can cover maximum possible of the stator faults. The fault considered in this study take into account a short circuit with large variations in the machine load. Moreover, the objective is to automate the diagnosis algorithm by using ANN classifier. Method. The database used for the ANN is based on indicators which are obtained from wavelet analysis of the machine stator current of one phase. The developed neural model allows to taking in consideration imbalances which are generated by short circuits in the machine stator. The implemented mathematical model in the expert system is based on a three-phase model. The mathematical parameters considered in this model are calculated online. The characteristic vector of the ANN model is formed by decomposition of stator current signal using wavelet discrete technique. Obtained results show that this technique allows to ensure more detection with clear evaluation of turn number in short circuit. Also, the developed expert system for the taken configurations is characterized by high precision.Вступ. Нині діагностика несправностей асинхронних машин відіграє значну роль у промисловості. У цій статті запропоновано модель штучної нейронної мережі для автоматичної діагностики несправностей асинхронної машини. Метою цього дослідження є розробка моделі нейронної мережі, що дозволяє генерувати велику базу даних. Ця база може охоплювати максимально можливі несправності статора. Несправності, розглянуті у цьому дослідженні, враховують коротке замикання при великих коливаннях навантаження машини. Крім того, мета полягає в тому, щоб автоматизувати алгоритм діагностики за допомогою класифікатора штучної нейронної мережі. Метод. База даних, що використовується для штучної нейронної мережі, заснована на показниках, отриманих в результаті вейвлет-аналізу струму статора машини однієї фази. Розроблена нейронна модель дозволяє враховувати дисбаланси, що виникають при коротких замиканнях у статорі машини. Реалізована математична модель в експертній системі ґрунтується на трифазній моделі. Математичні параметри, що враховуються в цій моделі, розраховуються онлайн. Характеристичний вектор моделі штучної нейронної мережі формується шляхом розкладання сигналу струму статора з використанням вейвлет-дискретного методу. Отримані результати показують, що дана методика дозволяє забезпечити більше виявлення з чіткою оцінкою числа витків при короткому замиканні. Також розроблена експертна система для конфігурацій, що приймаються, відрізняється високою точністю

Pinch-off syndrome ou syndrome de la Pince Costo-Claviculaire à propos de deux cas

La chambre à cathéter implantable est un outil essentiel tout le long de la maladie cancéreuse. Cependant, son utilisation expose à des complications qui peuvent être grave. La rupture du cathéter de la chambre implantable retrouvée dans l’abord veineux sousclavier, secondaire le plus souvent au syndrome de la pince costo-claviculaire ou pinch off qui se produit lorsque le cathéter est comprimé entre la clavicule et la première côte. Nous rapportons deux cas de pinch-off syndrome pour évaluer l’approche diagnostique et thérapeutique de cette complication

Phéochromocytome de découverte fortuite (à propos d’un cas)

Nous rapportons un cas inhabituel d’incidentalome surrénalien compliqué d’un état de choc après surrénalectomie lors d’une intervention pour néoplasie du bas rectum ; qui s’est avéré être un phéochromocytome. Ainsi, cette observation montre la nécessité d’une exploration hormonale systématique de tout incidentalome surrénalien , afin d'éviter tout incident pouvant être fatal

A C-terminal cysteine residue is required for peptide-based inhibition of the NGF/TrkA interaction at nM concentrations:implications for peptide-based analgesics

Inhibition of the NGF/TrkA interaction presents an interesting alternative to the use of non-steroidal anti-inflammatories and/or opioids for the control of inflammatory, chronic and neuropathic pain. Most prominent of the current approaches to this therapy is the antibody Tanezumab, which is a late-stage development humanized monoclonal antibody that targets NGF. We sought to determine whether peptides might similarly inhibit the NGF/TrkA interaction and so serve as future therapeutic leads. Starting from two peptides that inhibit the NGF/TrkA interaction, we sought to eliminate a cysteine residue close to the C-terminal of both sequences, by an approach of mutagenic analysis and saturation mutagenesis of mutable residues. Elimination of cysteine from a therapeutic lead is desirable to circumvent manufacturing difficulties resulting from oxidation. Our analyses determined that the cysteine residue is not required for NGF binding, but is essential for inhibition of the NGF/TrkA interaction at pharmacologically relevant peptide concentrations. We conclude that a cysteine residue is required within potential peptide-based therapeutic leads and hypothesise that these peptides likely act as dimers, mirroring the dimeric structure of the TrkA receptor

Measurement of the cross-section and charge asymmetry of WW bosons produced in proton-proton collisions at s=8\sqrt{s}=8 TeV with the ATLAS detector

This paper presents measurements of the $W^+ \rightarrow \mu^+\nu$ and $W^- \rightarrow \mu^-\nu$ cross-sections and the associated charge asymmetry as a function of the absolute pseudorapidity of the decay muon. The data were collected in proton--proton collisions at a centre-of-mass energy of 8 TeV with the ATLAS experiment at the LHC and correspond to a total integrated luminosity of 20.2~\mbox{fb^{-1}}. The precision of the cross-section measurements varies between 0.8% to 1.5% as a function of the pseudorapidity, excluding the 1.9% uncertainty on the integrated luminosity. The charge asymmetry is measured with an uncertainty between 0.002 and 0.003. The results are compared with predictions based on next-to-next-to-leading-order calculations with various parton distribution functions and have the sensitivity to discriminate between them.Comment: 38 pages in total, author list starting page 22, 5 figures, 4 tables, submitted to EPJC. All figures including auxiliary figures are available at https://atlas.web.cern.ch/Atlas/GROUPS/PHYSICS/PAPERS/STDM-2017-13

Search for chargino-neutralino production with mass splittings near the electroweak scale in three-lepton final states in √s=13 TeV pp collisions with the ATLAS detector

A search for supersymmetry through the pair production of electroweakinos with mass splittings near the electroweak scale and decaying via on-shell W and Z bosons is presented for a three-lepton final state. The analyzed proton-proton collision data taken at a center-of-mass energy of √s=13  TeV were collected between 2015 and 2018 by the ATLAS experiment at the Large Hadron Collider, corresponding to an integrated luminosity of 139  fb−1. A search, emulating the recursive jigsaw reconstruction technique with easily reproducible laboratory-frame variables, is performed. The two excesses observed in the 2015–2016 data recursive jigsaw analysis in the low-mass three-lepton phase space are reproduced. Results with the full data set are in agreement with the Standard Model expectations. They are interpreted to set exclusion limits at the 95% confidence level on simplified models of chargino-neutralino pair production for masses up to 345 GeV

A Dialogue between the Hypoxia-Inducible Factor and the Tumor Microenvironment

The hypoxia-inducible factor is the key protein responsible for the cellular adaptation to low oxygen tension. This transcription factor becomes activated as a result of a drop in the partial pressure of oxygen, to hypoxic levels below 5% oxygen, and targets a panel of genes involved in maintenance of oxygen homeostasis. Hypoxia is a common characteristic of the microenvironment of solid tumors and, through activation of the hypoxia-inducible factor, is at the center of the growth dynamics of tumor cells. Not only does the microenvironment impact on the hypoxia-inducible factor but this factor impacts on microenvironmental features, such as pH, nutrient availability, metabolism and the extracellular matrix. In this review we discuss the influence the tumor environment has on the hypoxia-inducible factor and outline the role of this factor as a modulator of the microenvironment and as a powerful actor in tumor remodeling. From a fundamental research point of view the hypoxia-inducible factor is at the center of a signaling pathway that must be deciphered to fully understand the dynamics of the tumor microenvironment. From a translational and pharmacological research point of view the hypoxia-inducible factor and its induced downstream gene products may provide information on patient prognosis and offer promising targets that open perspectives for novel “anti-microenvironment” directed therapies

Long-term exposure to hypoxia inhibits tumor progression of lung cancer in rats and mice

<p>Abstract</p> <p>Background</p> <p>Hypoxia has been identified as a major negative factor for tumor progression in clinical observations and in animal studies. However, the precise role of hypoxia in tumor progression has not been fully explained. In this study, we extensively investigated the effect of long-term exposure to hypoxia on tumor progression <it>in vivo.</it></p> <p>Methods</p> <p>Rats bearing transplanted tumors consisting of A549 human lung cancer cells (lung cancer tumor) were exposed to hypoxia for different durations and different levels of oxygen. The tumor growth and metastasis were evaluated. We also treated A549 lung cancer cells (A549 cells) with chronic hypoxia and then implanted the hypoxia-pretreated cancer cells into mice. The effect of exposure to hypoxia on metastasis of Lewis lung carcinoma in mice was also investigated.</p> <p>Results</p> <p>We found that long-term exposure to hypoxia a) significantly inhibited lung cancer tumor growth in xenograft and orthotopic models in rats, b) significantly reduced lymphatic metastasis of the lung cancer in rats and decreased lung metastasis of Lewis lung carcinoma in mice, c) reduced lung cancer cell proliferation and cell cycle progression <it>in vitro</it>, d) decreased growth of the tumors from hypoxia-pretreated A549 cells, e) decreased Na⁺-K⁺ATPase α1 expression in hypoxic lung cancer tumors, and f) increased expression of hypoxia inducible factors (HIF1α and HIF2α) but decreased microvessel density in the lung cancer tumors. In contrast to lung cancer, the growth of tumor from HCT116 human colon cancer cells (colon cancer tumor) was a) significantly enhanced in the same hypoxia conditions, accompanied by b) no significant change in expression of Na⁺-K⁺ATPase α1, c) increased HIF1α expression (no HIF2α was detected) and d) increased microvessel density in the tumor tissues.</p> <p>Conclusions</p> <p>This study demonstrated that long-term exposure to hypoxia repressed tumor progression of the lung cancer from A549 cells and that decreased expression of Na⁺-K⁺ATPase was involved in hypoxic inhibition of tumor progression. The results from this study provide new insights into the role of hypoxia in tumor progression and therapeutic strategies for cancer treatment.</p