Reação de genótipos de triticale (X Triticosecale Wittmack) e de centeio (Secale cereale L.) ao BYDV-PAV, agente causal do nanismo amarelo: análise de dados do ano de 2011.

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Quench propagation and detection in the superconducting bus-bars of the ATLAS magnets

The ATLAS superconducting magnet system comprising Barrel (BT) and End-Cap Toroids (ECT) and also Central Solenoid (CS) will store more than 1.5 GJ of magnetic energy. The magnet system will have many superconducting busbars, a few meters long each, running from the current leads to Central Solenoid and Toroids as well as between the coils of each Toroid. Quench development in the busbars, i.e., the normal zone propagation process along the busbar superconductors, is slow and exhibits very low voltages. Therefore, its timely and appropriate detection represents a real challenge. The temperature evolution in the busbars under quench is of primary importance. Conservative calculations of the temperature were performed for all the magnets. Also, a simple and effective method to detect a normal zone in a busbar is presented. A thin superconducting wire, whose normal resistance can be easily detected, is placed in a good thermal contact to busbar. Thus, the wire can operate as straightforward and low-noise quench-detector. (4 refs)

Manejo integrado de pragas de grãos armazenados.

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The ATLAS magnet test facility at CERN

The magnet system for the ATLAS detector at CERN consists of a Barrel Toroid (BT), two End-Cap Toroids (ECT) and a Central Solenoid (CS). The overall dimensions of the system are 20 m in diameter by 26 m in length. Before underground installation all coils will be tested on surface in a magnet test facility which is under construction. Moreover two model coils are tested as well as subsystems. In this paper the design and construction of the test facility is presented. (3 refs)

Status of the CMS magnet (MT17)

The CMS experiment (Compact Muon Solenoid) is a general-purpose detector designed to run at the highest luminosity at the CERN Large Hadron Collider (LHC). Its distinctive features include a 4 T superconducting solenoid with a free bore of 6 m diameter and 12.5-m length, enclosed inside a 10 000-ton return yoke. The magnet will be assembled and tested in a surface hall at Point 5 of the LHC at the beginning of 2004 before being transferred by heavy lifting means to an experimental hall 90 m below ground level. The design and construction of the magnet is a common project of the CMS Collaboration. The task is organized by a CERN based group with strong technical and contractual participation from CEA Saclay, ETH Zurich, Fermilab, INFN Genova, ITEP Moscow, University of Wisconsin and CERN. The magnet project will be described, with emphasis on the present status of the fabrication. (15 refs)

Pathogenic Mechanism of the FIG4 Mutation Responsible for Charcot-Marie-Tooth Disease CMT4J

CMT4J is a severe form of Charcot-Marie-Tooth neuropathy caused by mutation of the phosphoinositide phosphatase FIG4/SAC3. Affected individuals are compound heterozygotes carrying the missense allele FIG4-I41T in combination with a null allele. Analysis using the yeast two-hybrid system demonstrated that the I41T mutation impairs interaction of FIG4 with the scaffold protein VAC14. The critical role of this interaction was confirmed by the demonstration of loss of FIG4 protein in VAC14 null mice. We developed a mouse model of CMT4J by expressing a Fig4-I41T cDNA transgene on the Fig4 null background. Expression of the mutant transcript at a level 5× higher than endogenous Fig4 completely rescued lethality, whereas 2× expression gave only partial rescue, providing a model of the human disease. The level of FIG4-I41T protein in transgenic tissues is only 2% of that predicted by the transcript level, as a consequence of the protein instability caused by impaired interaction of the mutant protein with VAC14. Analysis of patient fibroblasts demonstrated a comparably low level of mutant I41T protein. The abundance of FIG4-I41T protein in cultured cells is increased by treatment with the proteasome inhibitor MG-132. The data demonstrate that FIG4-I41T is a hypomorphic allele encoding a protein that is unstable in vivo. Expression of FIG4-I41T protein at 10% of normal level is sufficient for long-term survival, suggesting that patients with CMT4J could be treated by increased production or stabilization of the mutant protein. The transgenic model will be useful for testing in vivo interventions to increase the abundance of the mutant protein

Inhibition of PIKfyve by YM-201636 Dysregulates Autophagy and Leads to Apoptosis-Independent Neuronal Cell Death

The lipid phosphatidylinositol 3,5-bisphosphate (PtdIns(3,5)P-2), synthesised by PIKfyve, regulates a number of intracellular membrane trafficking pathways. Genetic alteration of the PIKfyve complex, leading to even a mild reduction in PtdIns(3,5)P-2 results in marked neurodegeneration via an uncharacterised mechanism. In the present study we have shown that selectively inhibiting PIKfyve activity, using YM-201636, significantly reduces the survival of primary mouse hippocampal neurons in culture. YM-201636 treatment promoted vacuolation of endolysosomal membranes followed by apoptosis-independent cell death. Many vacuoles contained intravacuolar membranes and inclusions reminiscent of autolysosomes. Accordingly, YM-201636 treatment increased the level of the autophagosomal marker protein LC3-II, an effect that was potentiated by inhibition of lysosomal proteases, suggesting that alterations in autophagy could be a contributing factor to neuronal cell death

The PIKfyve Inhibitor YM201636 Blocks the Continuous Recycling of the Tight Junction Proteins Claudin-1 and Claudin-2 in MDCK cells

Tight junctions mediate the intercellular diffusion barrier found in epithelial tissues but they are not static complexes; instead there is rapid movement of individual proteins within the junctions. In addition some tight junction proteins are continuously being endocytosed and recycled back to the plasma membrane. Understanding the dynamic behaviour of tight junctions is important as they are altered in a range of pathological conditions including cancer and inflammatory bowel disease. In this study we investigate the effect of treating epithelial cells with a small molecule inhibitor (YM201636) of the lipid kinase PIKfyve, a protein which is involved in endocytic trafficking. We show that MDCK cells treated with YM201636 accumulate the tight junction protein claudin-1 intracellularly. In contrast YM201636 did not alter the localization of other junction proteins including ZO-1, occludin and E-cadherin. A biochemical trafficking assay was used to show that YM201636 inhibited the endocytic recycling of claudin-1, providing an explanation for the intracellular accumulation. Claudin-2 was also found to constantly recycle in confluent MDCK cells and treatment with YM201636 blocked this recycling and caused accumulation of intracellular claudin-2. However, claudin-4 showed negligible endocytosis and no detectable intracellular accumulation occurred following treatment with YM201636, suggesting that not all claudins show the same rate of endocytic trafficking. Finally, we show that, consistent with the defects in claudin trafficking, incubation with YM201636 delayed formation of the epithelial permeability barrier. Therefore, YM201636 treatment blocks the continuous recycling of claudin-1/claudin-2 and delays epithelial barrier formation

Arabidopsis AtVPS15 is essential for pollen development and germination through modulating phosphatidylinositol 3-phosphate formation

Arabidopsis thaliana phosphatidylinositol 3-kinase (AtVPS34) functions in the development and germination of pollen by catalyzing the biosynthesis of phosphatidylinositol 3-phosphate (PI3P). In yeast, Vps15p is required for the membrane targeting and activity of Vps34. The expression of Arabidopsis thaliana VPS15 (AtVPS15), an ortholog of yeast Vps15, is mainly detected in pollen grains and pollen tubes. To determine its role in pollen development and pollen tube growth, we attempted to isolate the T-DNA insertion mutants of AtVPS15; however, homozygous lines of atvps15 were not obtained from the progeny of atvps15/+ heterozygotes. Genetic analysis revealed that the abnormal segregation is due to the failure of transmission of the atvps15 allele through pollen. Most pollen grains from the atvps15/+ genotype are viable, with normal exine structure and nuclei, but some mature pollen grains are characterized with unusual large vacuoles that are not observed in pollen grains from the wild AtVPS15 genotype. The germination ratio of pollen from the atvps15/+ genotype is about half when compared to that from the wild AtVPS15 genotype. When supplied with PI3P, in vitro pollen germination of the atvps15/+ genotype is greatly improved. Presumably, AtVPS15 functions in pollen development and germination by regulating PI3P biosynthesis in Arabidopsis