Accidental Removal of a Carotid Endovascular Stent during Oropharyngeal Mass Biopsy

A 54-year-old male patient, with a history of a right mandibular adenocarcinoma, previously excised, and treated with post operative chemo- and radio-therapy, presented with a right oropharyngeal necrotic mass of several months duration. His history is pertinent for a right internal carotid endovascular stenting 2 years prior to presentation. During biopsy of his oropharyngeal lesion, a specimen of tissue was retrieved, with the carotid stent within. There was no bleeding. To the best of our knowledge, there is no such case reported in the literature. We present this case as a reminder on the importance and risks of radiation-induced necrosis and its distortion of the surrounding anatomy, especially in the presence of foreign bodies or protheses

La gestión pública de las prohibiciones alimentarias en Francia: El caso de la escuela y el hospital

Conferencia impartida en el Congreso Internacional Alimentación, creencias y diversidad cultural, celebrado en la Facultad de Derecho de la Universidad de León, del 8 al 10 de octubre de 2012

La gestión pública de las prohibiciones alimentarias en Francia: El caso de la escuela y el hospital

El Área de Derecho Eclesiástico del Estado, junto al Instituto Politécnico de Bragança (Portugal), en el marco del Proyecto “Campus de Excelencia Internacional de la Universidad de León CEI – ERMES” organiza un Congreso Internacional sobre “Alimentación, creencias y diversidad cultural” en el Salón de Grados de la Facultad de Derecho del 8 al 10 de octubre de 201

Pluri, multi-, trans-meta-and interdisciplinary nature of LIS. Does it really matter?

International audienceThe field of LIS is beset by recurrent debates as to its disciplinary status. For decades, the interdisciplinary nature of information science has been upheld without much proof from the ground. But if LIS is not an interdiscipline, is it then a meta-, a trans- a pluri-, a multi- or simply a discipline? The different proposals for qualifying the nature of LIS or for delineating its frontiers suggest that its fundamental nature remains unclear for its community. But is LIS alone in this dilemma and does it really matter? Does it stop the field from progressing

The PDE1/5 Inhibitor SCH-51866 Does Not Modify Disease Progression in the R6/2 Mouse Model of Huntington's Disease

Huntington’s disease is a neurodegenerative disorder caused by mutations in the CAG tract of huntingtin. Several studies in HD cellular and rodent systems have identified disturbances in cyclic nucleotide signaling, which might be relevant to pathogenesis and therapeutic intervention. To investigate whether selective phosphodiesterase (PDE) inhibitors can improve some aspects of disease pathogenesis in HD models, we have systematically evaluated the effects of a variety of cAMP and cGMP selective PDE inhibitors in various HD models. Here we present the lack of effect in a variety of endpoints of the PDE subtype selective inhibitor SCH-51866, a PDE1/5 inhibitor, in the R6/2 mouse model of HD, after chronic oral dosing

Noncanonical autophagy is required for type I interferon secretion in response to DNA-immune complexes.

Toll-like receptor-9 (TLR9) is largely responsible for discriminating self from pathogenic DNA. However, association of host DNA with autoantibodies activates TLR9, inducing the pathogenic secretion of type I interferons (IFNs) from plasmacytoid dendritic cells (pDCs). Here, we found that in response to DNA-containing immune complexes (DNA-IC), but not to soluble ligands, IFN-α production depended upon the convergence of the phagocytic and autophagic pathways, a process called microtubule-associated protein 1A/1B-light chain 3 (LC3)-associated phagocytosis (LAP). LAP was required for TLR9 trafficking into a specialized interferon signaling compartment by a mechanism that involved autophagy-related proteins, but not the conventional autophagic preinitiation complex, or adaptor protein-3 (AP-3). Our findings unveil a new role for nonconventional autophagy in inflammation and provide one mechanism by which anti-DNA autoantibodies, such as those found in several autoimmune disorders, bypass the controls that normally restrict the apportionment of pathogenic DNA and TLR9 to the interferon signaling compartment

Quantification Assays for Total and Polyglutamine-Expanded Huntingtin Proteins

<div><p>The expansion of a CAG trinucleotide repeat in the huntingtin gene, which produces huntingtin protein with an expanded polyglutamine tract, is the cause of Huntington's disease (HD). Recent studies have reported that RNAi suppression of polyglutamine-expanded huntingtin (mutant HTT) in HD animal models can ameliorate disease phenotypes. A key requirement for such preclinical studies, as well as eventual clinical trials, aimed to reduce mutant HTT exposure is a robust method to measure HTT protein levels in select tissues. We have developed several sensitive and selective assays that measure either total human HTT or polyglutamine-expanded human HTT proteins on the electrochemiluminescence Meso Scale Discovery detection platform with an increased dynamic range over other methods. In addition, we have developed an assay to detect endogenous mouse and rat HTT proteins in pre-clinical models of HD to monitor effects on the wild type protein of both allele selective and non-selective interventions. We demonstrate the application of these assays to measure HTT protein in several HD <i>in vitro</i> cellular and <i>in vivo</i> animal model systems as well as in HD patient biosamples. Furthermore, we used purified recombinant HTT proteins as standards to quantitate the absolute amount of HTT protein in such biosamples.</p></div

Specificity of human mutant and mouse HTT detection.

<p>The adeno-associated AAV-shRNA expression vector AAV-SEWB-sh4 was transduced into heterozygous zQ175 mouse primary neurons and humanized mutant (A) or endogenous mouse (B) HTT proteins were evaluated using the expanded polyglutamine human HTT MSD assay (antibody pair pAb146/MW1) or the mouse/rat HTT MSD assay (antibody pair pAb147/MAB2166), respectively. sh4, <i>HTT</i> targeting shRNA. scr6, scramble control shRNA. (C) Neuronal total tau protein levels measured using a commercially available MSD ELISA-based assay kit were monitored as loading control. Data are averages of n = 3 independent samples with correspondent standard deviations. ***, P<0.001. (D) Immunoblot confirming the AAV-mediated knockdown of humanized mutant (mut) and endogenous mouse HTT in transduced heterozygous zQ175 mouse primary neurons (AAV-SEWB-sh4: <i>HTT</i> targeting shRNA; AAV-SEWB-scr6: scrambled control shRNA). Immunoblot was probed for HTT (MAB2166, 1∶1,000; Millipore) or ATP5B as loading control.</p

Decrease of soluble mutant HTT levels in R6/2 brain tissues is associated with increased age of the mice.

<p>(A) Homogenates from brains of R6/2 female mice obtained from The Jackson Laboratory (bearing an expanded polyglutamine tract of 120 CAG repeats on average) were analyzed for detection of soluble mutant human HTT at different ages (4, 8 and 12 weeks). Tissues analyzed showed significant signals in the expanded polyglutamine human HTT MSD assay (antibody pair pAb146/MW1) and a significant signal decrease between 4 and 8 weeks of age. Data are averages of n = 4 independent samples with correspondent standard deviations. B, assay background. ***, P<0.001. (B) SDS-PAGE and immunoblotting for HTT with the MW8 antibody reveals high molecular weight bands (presumably HTT aggregates) in R6/2 brain homogenates that increase with increasing age of the animals. Progressive decrease of soluble monomeric HTT fragments can be observed. WT, wild type (CBA×C57Bl/6) F1 (CBF) (B6CBAF1/OlaHsd, Harlan Olac) mice.</p