641 research outputs found

    Noxiousness of the african white stem borer, Maliarpha separatella Rag (Pyralidae: Phycitinae) in irrigated paddy fields at lake Alaotra (Madagascar)

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    A study of the noxiousness of the African white rice stem borer, Maliarpha separatella Rag carried out under controlled field conditions has revealed that the impact of this pest on the yield and its components is assessable. For mean infestation rates up to 68% during the period of highest sensitivity of a paddy rice culture (second half of tillering to panicle initiation), no significant decrease could be observed in the number of panicles, nor any significant increase in the number of white heads and the number of empty grains per hill. However, with increasing infestation rates, the number of immature panicles increased and the number and weight of filled grains per hill decreased. An explorative analysis of the infestation rate-yield loss relationship, showed that a sigmoid model describes this interdependence appropriately. The proposed economic injury level (EIL), is here considered more the result of an approach, which had as its goal the re-definition of the status of the pest than as an instrument of a chemical control programme with treatments based on an action threshol

    Arthrogryposis multiplex congenita (AMC), a hereditary disease in swine, maps to Chromosome 5 by linkage analysis

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    Arthrogryposis multiplex congenita (AMC), defined as permanent joint contractures present at birth, is one of the most common congenital defects in piglets and other mammals. A genetic form of arthrogryposis was recently identified in Swiss Large White (LW) pigs. The disease is controlled by a single autosomal recessive allele designated as amc. At least 14 LW AI (artificial insemination) boars (about 25% of the Swiss population) are known to be carriers of the amc allele. A total of 219 pigs were used for linkage analysis, including seven founders (F1), three F0, 160 F2, and 49 F3 animals. All founder pigs were full or half sibs. Of the 219 pigs, 41 (18.7%) were found to be affected, while the remaining 178 (81.3%) were healthy. A comprehensive genome scan revealed that microsatellite SW1987 located on pig (Sus scrofa) Chromosome 5 (SSC5), was linked with AMC. Sixteen additional SSC5 microsatellites were selected for further genotyping to generate a multipoint map covering the AMC region. Significant pairwise linkage (LOD > 6.00) was found for AMC and eight marker loci. The order that best fit with the data was SW963-SW1987-SW152-AMC-(SW904, SW1094)-SWR1526-(SWR1974, SW310). AMC was mapped by linkage analysis to the position 92cM, between SW152 and SW904/SW1094, which are located on SSC5 in bands q12-q2

    EU and NATO: the legal foundation of an extraordinary partnership

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    The EU and NATO are historic partners. Since the end of the last century, both organisations have worked together in the field of defence to ensure peace and security on the European continent. Common values and challenges have made their partnership one of the most successful in the world. However, the EU-NATO relationship has traditionally been legally unclear and not fully operational, with stops and starts. In particular, NATO seemed lost after the disintegration of the Union of Soviet Socialist Republics, and the EU has never proved to have sufficient military capabilities to play a security role on its own. This article seeks to understand the legal basis of the EU-NATO partnership, with the ultimate aim of demonstrating that it has been effective throughout history. It tries to systematise the legal acts of both organisations in a new and coherent way, revealing the extraordinary nature of this relationship. As this contribution argues, EU-NATO cooperation is not only legally anchored in the meaning of the EU and NATO Treaties. Still, it is also put into practice through mutual participation in their respective fields of action

    Impact of sequence variation in the ul128 locus on production of human cytomegalovirus in fibroblast and epithelial cells

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    The human cytomegalovirus (HCMV) virion envelope contains a complex consisting of glycoproteins gH and gL plus proteins encoded by the UL128 locus (UL128L): pUL128, pUL130, and pUL131A. UL128L is necessary for efficient infection of myeloid, epithelial, and endothelial cells but limits replication in fibroblasts. Consequently, disrupting mutations in UL128L are rapidly selected when clinical isolates are cultured in fibroblasts. In contrast, bacterial artificial chromosome (BAC)-cloned strains TB40-BAC4, FIX, and TR do not contain overt disruptions in UL128L, yet no virus reconstituted from them has been reported to acquire mutations in UL128L in vitro. We performed BAC mutagenesis and reconstitution experiments to test the hypothesis that these strains contain subtle mutations in UL128L that were acquired during passage prior to BAC cloning. Compared to strain Merlin containing wild-type UL128L, all three strains produced higher yields of cell-free virus. Moreover, TB40-BAC4 and FIX spread cell to cell more rapidly than wild-type Merlin in fibroblasts but more slowly in epithelial cells. The differential growth properties of TB40-BAC4 and FIX (but not TR) were mapped to single-nucleotide substitutions in UL128L. The substitution in TB40-BAC4 reduced the splicing efficiency of UL128, and that in FIX resulted in an amino acid substitution in UL130. Introduction of these substitutions into Merlin dramatically increased yields of cell-free virus and increased cell-to-cell spread in fibroblasts but reduced the abundance of pUL128 in the virion and the efficiency of epithelial cell infection. These substitutions appear to represent mutations in UL128L that permit virus to be propagated in fibroblasts while retaining epithelial cell tropism

    Up-Regulation of Tumor Necrosis Factor Superfamily Genes in Early Phases of Photoreceptor Degeneration

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    We used quantitative real-time PCR to examine the expression of 112 genes related to retinal function and/or belonging to known pro-apoptotic, cell survival, and autophagy pathways during photoreceptor degeneration in three early-onset canine models of human photoreceptor degeneration, rod cone dysplasia 1 (rcd1), X-linked progressive retinal atrophy 2 (xlpra2), and early retinal degeneration (erd), caused respectively, by mutations in PDE6B, RPGRORF15, and STK38L. Notably, we found that expression and timing of differentially expressed (DE) genes correlated with the cell death kinetics. Gene expression profiles of rcd1 and xlpra2 were similar; however rcd1 was more severe as demonstrated by the results of the TUNEL and ONL thickness analyses, a greater number of genes that were DE, and the identification of altered expression that occurred at earlier time points. Both diseases differed from erd, where a smaller number of genes were DE. Our studies did not highlight the potential involvement of mitochondrial or autophagy pathways, but all three diseases were accompanied by the down-regulation of photoreceptor genes, and up-regulation of several genes that belong to the TNF superfamily, the extrinsic apoptotic pathway, and pro-survival pathways. These proteins were expressed by different retinal cells, including horizontal, amacrine, ON bipolar, and Müller cells, and suggest an interplay between the dying photoreceptors and inner retinal cells. Western blot and immunohistochemistry results supported the transcriptional regulation for selected proteins. This study highlights a potential role for signaling through the extrinsic apoptotic pathway in early cell death events and suggests that retinal cells other than photoreceptors might play a primary or bystander role in the degenerative process

    Multiple Interactions between Peroxisome Proliferators-Activated Receptors and the Ubiquitin-Proteasome System and Implications for Cancer Pathogenesis

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    The peroxisome proliferator-activated receptors (PPAR) α, β/δ, and γ are ligand-activated nuclear receptors involved in a number of physiological processes, including lipid and glucose homeostasis, inflammation, cell growth, differentiation, and death. PPAR agonists are used in the treatment of human diseases, like type 2 diabetes and dyslipidemia, and PPARs appear as promising therapeutic targets in other conditions, including cancer. A better understanding of the functions and regulation of PPARs in normal and pathological processes is of primary importance to devise appropriate therapeutic strategies. The ubiquitin-proteasome system (UPS) plays an important role in controlling level and activity of many nuclear receptors and transcription factors. PPARs are subjected to UPS-dependent regulation. Interestingly, the three PPAR isotypes are differentially regulated by the UPS in response to ligand-dependent activation, a phenomenon that may be intrinsically connected to their distinct cellular functions and behaviors. In addition to their effects ongene expression, PPARs appear to affect protein levels and downstream pathways also by modulating the activity of the UPS in target-specific manners. Here we review the current knowledge of the interactions between the UPS and PPARs in light of the potential implications for their effects on cell fate and tumorigenesis
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