101 research outputs found

    Measurement of differential cross sections for Z boson pair production in association with jets at root s=8 and 13 TeV

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    This Letter reports measurements of differential cross sections for the production of two Z bosons in association with jets in proton-proton collisions at root s = 8 and 13 TeV. The analysis is based on data samples collected at the LHC with the CMS detector, corresponding to integrated luminosities of 19.7 and 35.9 fb(-1) at 8 and 13 TeV, respectively. The measurements are performed in the leptonic decay modes ZZ -> l(+)l(-)l'(+)l'(-), where, l, l' = e, mu The differential cross sections as a function of the jet multiplicity, the transverse momentum p(T), and pseudorapidity of the P-T-leading and subleading jets are presented. In addition, the differential cross sections as a function of variables sensitive to the vector boson scattering, such as the invariant mass of the two P-T-leading jets and their pseudorapidity separation, are reported. The results are compared to theoretical predictions and found in good agreement within the theoretical and experimental uncertainties. (C) 2018 The Author(s). Published by Elsevier B.V.Peer reviewe

    Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

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    In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

    Introduction to the physics of the total cross section at LHC

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    Differential Contribution of L-, N-, and P/Q-type Calcium Channels to [Ca2+]i Changes Evoked by Kainate in Hippocampal Neurons

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    Abstract We investigated the contribution of L-, N- and P/Q-type Ca2+ channels to the [Ca2+]i changes, evoked by kainate, in the cell bodies of hippocampal neurons, using a pharmacological approach and Ca2+ imaging. Selective Ca2+ channel blockers, namely nitrendipine, ?-Conotoxin GVIA (?-GVIA) and ?-Agatoxin IVA (?-AgaIVA) were used. The [Ca2+]i changes evoked by kainate presented a high variability, and were abolished by NBQX, a AMPA/kainate receptor antagonist, but the N-methyl-d-aspartate (NMDA) receptor antagonist, D-AP5, was without effect. Each Ca2+ channel blocker caused differential inhibitory effects on [Ca2+]i responses evoked by kainate. We grouped the neurons for each blocker in three subpopulations: (1) neurons with responses below 60% of the control; (2) neurons with responses between 60% and 90% of the control, and (3) neurons with responses above 90% of the control. The inhibition caused by nitrendipine was higher than the inhibition caused by ?-GVIA or ?-AgaIVA. Thus, in the presence of nitrendipine, the percentage of cells with responses below 60% of the control was 41%, whereas in the case of ?-GVIA or ?-AgaIVA the values were 9 or 17%, respectively. The results indicate that hippocampal neurons differ in what concerns their L-, N- and P/Q- type Ca2+ channels activated by stimulation of the AMPA/kainate receptors
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