Metodo per la diagnosi ed il monitoraggio della celiachia su campioni di saliva (Methods for the diagnosis and monitoring of Celiac Disease in Saliva Samples).

La presente invenzione riguarda un metodo per la diagnosi ed il monitoraggio della celiachia, in particolare attraverso la determinazione di anticorpi anti-transglutaminasi tissutale (IgA anti-tTG). Nello specifico, detto metodo si applica su 10 campioni di saliva mediante l’impiego di un immunosensore elettrochimico in grado di rilevare gli anticorpi IgA anti-tTG

Experimental validation.

<p>a) Network of high scoring associations around the PROKR2 gene. PROKR2 is linked to the anabolic steroids <i>oxandrolone</i> and <i>oxymetholone</i>. The androgen receptor (AR) exhibits a high phenotypic similarity to known direct (blue) and indirect (green) targets of AR. The coloured hexagons indicate the pharmacological subgroup of the ATC classification system. b) Dose response curve of <i>oxandrolone</i> on the PKR₂ antagonistic assay. Two replicate measurements, their average and the fitted dose-response curve are shown.</p

Network of high scoring biological-gene associations.

<p>The network of high scoring biological-gene connections is shown and some associations that are discussed in more detail in the manuscript are highlighted in a zoom-in. The follicle stimulating hormone receptor is e.g. connected to <i>follitropin beta</i>, a recombinant form of follicle stimulating hormone (FSH) or genes encoding for proteins that are members of the coagulation cascade are linked to anticoagulants like <i>lutropin alpha</i>.</p

Examples of high-scoring gene-drug associations mentioned throughout the text.

<p>Information about the associated phenotypic similarity score and the precision (%) based on the benchmarking results with direct drug targets of STITCH is included. (B) indicates that this drug is a biological.</p

Rapamycin and fasting sustain autophagy response activated by ischemia/reperfusion injury and promote retinal ganglion cell survival

Abstract Autophagy, the cellular process responsible for degradation and recycling of cytoplasmic components through the autophagosomal–lysosomal pathway, is fundamental for neuronal homeostasis and its deregulation has been identified as a hallmark of neurodegeneration. Retinal hypoxic–ischemic events occur in several sight-treating disorders, such as central retinal artery occlusion, diabetic retinopathy, and glaucoma, leading to degeneration and loss of retinal ganglion cells. Here we analyzed the autophagic response in the retinas of mice subjected to ischemia induced by transient elevation of intraocular pressure, reporting a biphasic and reperfusion time-dependent modulation of the process. Ischemic insult triggered in the retina an acute induction of autophagy that lasted during the first hours of reperfusion. This early upregulation of the autophagic flux limited RGC death, as demonstrated by the increased neuronal loss observed in mice with genetic impairment of basal autophagy owing to heterozygous ablation of the autophagy-positive modulator Ambra1 (Ambra1 +/gt ). Upregulation of autophagy was exhausted 24 h after the ischemic event and reduced autophagosomal turnover was associated with build up of the autophagic substrate SQSTM-1/p62, decreased ATG12-ATG5 conjugate, ATG4 and BECN1/Beclin1 expression. Animal fasting or subchronic systemic treatment with rapamycin sustained and prolonged autophagy activation and improved RGC survival, providing proof of principle for autophagy induction as a potential therapeutic strategy in retinal neurodegenerative conditions associated with hypoxic/ischemic stresses

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field