224 research outputs found

    Heraldic seizure

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    AbstractBackground: The term heraldic seizures indicates epileptic seizures caused by cerebrovascular disease, believed to be triggered by silent ischemia and occurring before a stroke. This fact widens the spectrum of possible interrelations between epilepsy and cerebrovascular disease outside the well known context of post-stroke epilepsy. Methods: This is a case report of a healthy 67-year-old male who had a new onset epileptic seizure prior to a lobar intracerebral hemorrhage (ICH). This man began to suffer myoclonic jerks in his left arm which progressed to a generalized tonic–clonic seizure. At the emergency area the physical and neurological examination were unremarkable and a CT scan was normal. The next day the patient developed left hemiparesis, hemianopsia and confusion and a new CT scan showed right parietal–occipital ICH. Conclusions: This case report exemplifies the concept of heraldic seizures, showing a patient who had a focal seizure preceding an intracerebral hemorrhage. Our etiologic diagnostic work led us to a diagnosis of probable amyloid angiopathy. We suggest that cerebral amyloid angiopathy (CAA) may be the underlying cause, since it may be the origin of both the late event (ICH) and the heralding seizures, resulting from concurrent ischemia

    Technical note:The persistence of microbial-specific DNA sequences through gastric digestion in lambs and its potential use as microbial markers

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    Two groups of 5 lambs were euthanized at the weaning (T45) and fattening stages (T90) to evaluate the use of microbial ribosomal DNA (rDNA) sequences as potential microbial markers in relation to purine bases (PB) as a conventional marker. Both microbial markers originated similar microbial N concentrations (mg/g of DM), although T45 showed decreased values compared with the T90 group when either PB or rDNA were considered (P = 0.02). The survival of microbial rDNA was determined in 3 digestive sites (omasum, abomasum, and duodenum), but no substantial differences were observed, indicating that rDNA maintains the molecular stability along the sampling sites analyzed. Contrarily PB concentration increased successively along the digestive tract (P < 0.05), likely as a consequence of the endogenous PB secretion. Undegraded milk PB may also explain the overestimation of the microbial N concentration (2.8 times greater) using PB than rDNA sequences. Abomasum was the sampling site where the best agreement between PB and rDNA estimations was observed. Protozoal N concentration was irrelevant in T45 animals, although substantial in T90 lambs (18% of microbial N). In conclusion, bacterial 16S and protozoal 18S rDNA sequences may persist through the gastric digestive tract and their utilization as a highly specific microbial marker should not be neglected.This study was supported by a FPU grant from the Education and Science Spanish Ministry (project: AGL 2004-02910/GAN) and by a University of Zaragoza project (UZ2008-BIO-04)

    Tracing KAM tori in presymplectic dynamical systems

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    We present a KAM theorem for presymplectic dynamical systems. The theorem has a " a posteriori " format. We show that given a Diophantine frequency ω\omega and a family of presymplectic mappings, if we find an embedded torus which is approximately invariant with rotation ω\omega such that the torus and the family of mappings satisfy some explicit non-degeneracy condition, then we can find an embedded torus and a value of the parameter close to to the original ones so that the torus is invariant under the map associated to the value of the parameter. Furthermore, we show that the dimension of the parameter space is reduced if we assume that the systems are exact.Comment: 33 pages and one figur

    Potential-density pairs for axisymmetric galaxies: the influence of scalar fields

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    We present a formulation for potential-density pairs to describe axisymmetric galaxies in the Newtonian limit of scalar-tensor theories of gravity. The scalar field is described by a modified Helmholtz equation with a source that is coupled to the standard Poisson equation of Newtonian gravity. The net gravitational force is given by two contributions: the standard Newtonian potential plus a term stemming from massive scalar fields. General solutions have been found for axisymmetric systems and the multipole expansion of the Yukawa potential is given. In particular, we have computed potential-density pairs of galactic disks for an exponential profile and their rotation curves.Comment: 8 pages, no figures, corrected version to the one that will appear in Gen. Relativ. Gravit., where a small typo in eq. (13) is presen

    Effect of the growth temperature and the AlN mole fraction on In incorporation and properties of quaternary III-nitride layers grown by molecular beam epitaxy

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    Indium incorporation into wurtzite (0001)-oriented InxAlyGa1−x−yN layers grown by plasma-assisted molecular beam epitaxy was studied as a function of the growth temperature (565–635 °C) and the AlN mole fraction (0.01<y<0.27). The layer stoichiometry was determined by Rutherford backscattering spectrometry (RBS). RBS shows that indium incorporation decreased continuously with increasing growth temperature due to thermally enhanced dissociation of In–N bonds and for increasing AlN mole fractions. High resolution x-ray diffraction and transmission electron microscopy (TEM) measurements did not show evidence of phase separation. The mosaicity of the quaternary layers was found to be mainly determined by the growth temperature and independent on alloy composition within the range studied. However, depending on the AlN mole fraction, nanometer-sized composition fluctuations were detected by TEM. Photoluminescence spectra showed a single broad emission at room temperature, with energy and bandwidth S- and W-shaped temperature dependences typical of exciton localization by alloy inhomogeneities. Cathodoluminescence measurements demonstrated that the alloy inhomogeneities, responsible of exciton localization, occur on a lateral length scale below 150 nm, which is corroborated by TE

    HER2 Oncogenic Function Escapes EGFR Tyrosine Kinase Inhibitors via Activation of Alternative HER Receptors in Breast Cancer Cells

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    BACKGROUND: The response rate to EGFR tyrosine kinase inhibitors (TKIs) may be poor and unpredictable in cancer patients with EGFR expression itself being an inadequate response indicator. There is limited understanding of the mechanisms underlying this resistance. Furthermore, although TKIs suppress the growth of HER2-overexpressing breast tumor cells, they do not fully inhibit HER2 oncogenic function at physiological doses. METHODOLOGY AND PRINCIPAL FINDINGS: Here we have provided a molecular mechanism of how HER2 oncogenic function escapes TKIs' inhibition via alternative HER receptor activation as a result of autocrine ligand release. Using both Förster Resonance Energy Transfer (FRET) which monitors in situ HER receptor phosphorylation as well as classical biochemical analysis, we have shown that the specific tyrosine kinase inhibitors (TKIs) of EGFR, AG1478 and Iressa (Gefitinib) decreased EGFR and HER3 phosphorylation through the inhibition of EGFR/HER3 dimerization. Consequent to this, we demonstrate that cleavage of HER4 and dimerization of HER4/HER2 occur together with reactivation of HER3 via HER2/HER3, leading to persistent HER2 phosphorylation in the now resistant, surviving cells. These drug treatment-induced processes were found to be mediated by the release of ligands including heregulin and betacellulin that activate HER3 and HER4 via HER2. Whereas an anti-betacellulin antibody in combination with Iressa increased the anti-proliferative effect in resistant cells, ligands such as heregulin and betacellulin rendered sensitive SKBR3 cells resistant to Iressa. CONCLUSIONS AND SIGNIFICANCE: These results demonstrate the role of drug-induced autocrine events leading to the activation of alternative HER receptors in maintaining HER2 phosphorylation and in mediating resistance to EGFR tyrosine kinase inhibitors (TKIs) in breast cancer cells, and hence specify treatment opportunities to overcome resistance in patients

    Epigenetic loss of RNA-methyltransferase NSUN5 in glioma targets ribosomes to drive a stress adaptive translational program

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    Altres ajuts: This work was supported by the Obra Social "La Caixa" (to M. Esteller).Tumors have aberrant proteomes that often do not match their corresponding transcriptome profiles. One possible cause of this discrepancy is the existence of aberrant RNA modification landscapes in the so-called epitranscriptome. Here, we report that human glioma cells undergo DNA methylation-associated epigenetic silencing of NSUN5, a candidate RNA methyltransferase for 5-methylcytosine. In this setting, NSUN5 exhibits tumor-suppressor characteristics in vivo glioma models. We also found that NSUN5 loss generates an unmethylated status at the C3782 position of 28S rRNA that drives an overall depletion of protein synthesis, and leads to the emergence of an adaptive translational program for survival under conditions of cellular stress. Interestingly, NSUN5 epigenetic inactivation also renders these gliomas sensitive to bioactivatable substrates of the stress-related enzyme NQO1. Most importantly, NSUN5 epigenetic inactivation is a hallmark of glioma patients with long-term survival for this otherwise devastating disease
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