Maize seed orientation in the substrate and its influences on germination, seedling structure, and transmission of Fusarium moniliforme

A research paper on maize seed orientation.The percentage of seedlings emerging during the first 4 days after sowing and the mesocotyl length after 7 days in sand at 25°C was strongly influenced by the orientation of the seed in the seedbed. Maize seeds emerged faster when oriented vertically with the pedicel end facing down (VD) or horizontally with the embryal side facing up (HU). The mesocotyl portion of the seedling was shorter (t 1mm) when sown at HU and VD, providing a fast and easy emergence to the seedling. It was much longer (20mm) when the seed was oriented horizontally with the embryal side facing down (HD) and vertically with the pedicel end facing up (VU). We concluded that the length of the mesocotyl portion of the seedling varies with the orientation of the seed in the substrate at the same depth. The seeds sown in the orientation HU and VU disclosed a higher germination of 95 percent and 88 percent respectively, compared to the seeds sown in the orientation HD and VD which had 68 percent and 53 percent germination respectively. Seed to seedling transmission of Fusarium moniliforme was recorded at a ratio of 1:1 in the untreated seeds, and infection of the fungus was found in the third leaf lamina and other sections of 10 day old seedlings. This demonstrates for the first time the systemic development of F. moniliforme above the crown portion of 10 day old seedlings. Treatment with Thiram contact fungicide improves the germination of highly infected seeds and also reduces the seed to seedling transmission of F. moniliforme. The efficiency of this seed treatment depended on the orientation of the seeds in the seedbed

Que valent les engagements des régimes de retraite envers les retraités en France ?

Using the "Echantillon Inter régimes des Retraités" (EIR) 2008 and 2012 panel data, we calculate retirees\u27 pension wealth (consumed and residual) at an aggregated level, and provide in-depth results by type of pension scheme and by managing organism. We put an emphasis on direct pensions already perceived by retirees and to be paid in the future, without taking into account current contributors\u27 future retirement. We find that the overall pension wealth is not very sensitive to the discount rate, but this result does not hold if we concentrate on the future pension wealth. From this point of view, it must be noted that some of the organisms have a high proportion of pension still to be paid. Moreover, whatever the type of pension wealth calculated, the results show a rapid increase from 2008 to 2012 (except for the basic scheme of farmers). Finally, spread indicators and Gini index of pension wealth are relatively higher than those found in the distribution of labor income by other studies. We find that there are more inequalities in the private sector than in the public, particularly in the private sector for complementary pension schemes

La réforme des retraites de 1993 : quel impact sur l'équivalent patrimonial des droits à retraite ?

Depuis 1993, la France a enregistré plusieurs réformes de son système de retraites, visant avant tout à en assurer la soutenabilité. Cette contribution a pour objectif d’évaluer l’impact de la réforme de 1993 sur l’équivalent patrimonial des droits individuels à la retraite (EPDR), c\u27est-à-dire la somme actuarielle probable des pensions à recevoir, de la date de liquidation des droits jusqu’au décès. Plus précisément, nous mesurons l’impact de cette réforme sur l’EPDR des mono-pensionnés du régime général, à l’aide des données de l’Echantillon Interrégimes de Retraités 2008. Parmi les mesures phares de la réforme de 1993 figure l’augmentation progressive de la durée de cotisation nécessaire pour obtenir une retraite à taux plein au régime général. Cette augmentation est susceptible d’engendrer deux effets opposés : un effet de report de l’âge de liquidation pour conserver un EPDR adéquat pour ses vieux jours (voire l’augmenter) ou un effet de décote, si l’assuré-e ne souhaite, ou ne peut, pas prolonger son activité et subit donc une décote sur sa pension, et partant sur son EPDR. Pour tester les effets nets de la réforme de 1993 sur l’EPDR, nous procédons à des estimations économétriques en différences premières et en doubles différences, ainsi qu’à des estimations par quantiles pour mesurer les impacts le long de la distribution de l’EPDR. Nos estimations montrent des résultats différents selon que les individus partent avant ou après 2004, date d’entrée en vigueur de la réforme. Ainsi, toutes choses égales par ailleurs, un départ en retraite avant 2004 plutôt que postérieurement, augmente l’EPDR des retraités concernés. Toutefois, l’interaction avec les autres variables nuance cette conclusion. D’une part, reporter son départ en retraite réduit l’EPDR moyen d’environ 20% : le report permet d’accumuler des droits supplémentaires, mais sur une période réduite. D’autre part, l’effet de la décote est négatif, mais son intensité est réduite quand les retraités reportent leur départ. En outre, comme les générations 1934-1943 ont subi conjointement les réformes de 1993 et 2003, nos estimations en double différence permettent d’isoler l’effet « pur » de la réforme de 1993 : lorsque les affiliés ont subi une décote, sans avoir reporté leur départ en retraite pour l’atténuer, la liquidation des droits aux conditions de 2003 par rapport aux conditions de 1993 est la plus défavorable. Enfin, les estimations par quantiles montrent que ces effets s’intensifient dans la première moitié de la distribution, et s’atténuent au-delà

Pension Wealth in France: An Assessment on Panel Data

This contribution proposes a measure of pension wealth in the French public PAYG schemes (first and second pillar schemes) and of its distribution among the population of retirees in 2008 using the Echantillon Inter régimes de Retraités (EIR) panel data. We show that aggregate pension wealth amounts to around 4765 billion Euros assuming a 2 percent discount rate. There are significant differences in the amount of individual’s pension wealth between the pension schemes of the private and public sector. Moreover, there is more inequality in the distribution of pension wealth among private sector retirees than public sectorones

Equivalent Patrimonial des Droits à Retraite en France : Méthodologie et Mesure dans l'EIR

L’équivalent patrimonial des droits à retraite (directs ou dérivés) permet d’évaluer la soutenabilité et la générosité des régimes de retraite. A l’aide des données de l’Echantillon Inter-régimes des Retraités de 2008, nous proposons une mesure de cet indicateur pour les assurés à la retraite du système de retraite français. L’objectif de cet article est de discuter des choix méthodologiques retenus à chaque étape de calcul de l’équivalent patrimonial et de souligner les contraintes et les limites spécifiques à un tel exercice. Les résultats obtenus révèlent que les différences entre les régimes de retraite peuvent générer des engagements d’une ampleur variable envers les assurés à la retraite. L’analyse de la concentration montre que la distribution de l’équivalent patrimonial des droits directs est plus inégale entre les assurés aux régimes complémentaires qu’entre les assurés des régimes de base ou intégrés (régime général, SRE-civile par exemple). Les inégalités au sein des régimes et entre les générations dans la distribution de l’équivalent patrimonial tendent globalement à diminuer au fil des générations étudiées

NAAA-regulated lipid signaling governs the transition from acute to chronic pain

Chronic pain affects 1.5 billion people worldwide but remains woefully undertreated. Understanding the molecular events leading to its emergence is necessary to discover disease-modifying therapies. Here we show that N-acylethanolamine acid amidase (NAAA) is a critical control point in the progression to pain chronicity, which can be effectively targeted by small-molecule therapeutics that inhibit this enzyme. NAAA catalyzes the deactivating hydrolysis of palmitoylethanolamide, a lipid-derived agonist of the transcriptional regulator of cellular metabolism, peroxisome proliferator-activated receptor-α (PPAR-α). Our results show that disabling NAAA in spinal cord during a 72-h time window following peripheral tissue injury halts chronic pain development in male and female mice by triggering a PPAR-α-dependent reprogramming of local core metabolism from aerobic glycolysis, which is transiently enhanced after end-organ damage, to mitochondrial respiration. The results identify NAAA as a crucial control node in the transition to chronic pain and a molecular target for disease-modifying medicines

Transcription factor and microRNA interactions in lung cells: an inhibitory link between NK2 homeobox 1, miR-200c and the developmental and oncogenic factors Nfib and Myb

Background: The transcription factor NK2 homeobox 1 (Nkx2-1) plays essential roles in epithelial cell proliferation and differentiation in mouse and human lung development and tumorigenesis. A better understanding of genes and pathways downstream of Nkx2-1 will clarify the multiple roles of this critical lung factor. Nkx2-1 regulates directly or indirectly numerous protein-coding genes; however, there is a paucity of information about Nkx2-1-regulated microRNAs (miRNAs). Methods and results: By miRNA array analyses of mouse epithelial cell lines in which endogenous Nkx2-1 was knocked-down, we revealed that 29 miRNAs were negatively regulated including miR-200c, and 39 miRNAs were positively regulated by Nkx2-1 including miR-1195. Mouse lungs lacking functional phosphorylated Nkx2-1 showed increased expression of miR-200c and alterations in the expression of other top regulated miRNAs. Moreover, chromatin immunoprecipitation assays showed binding of NKX2-1 protein to regulatory regions of these miRNAs. Promoter reporter assays indicated that 1kb of the miR-200c 5′ flanking region was transcriptionally active but did not mediate Nkx2-1- repression of miR-200c expression. 3′UTR reporter assays support a direct regulation of the predicted targets Nfib and Myb by miR-200c. Conclusions: These studies suggest that Nkx2-1 controls the expression of specific miRNAs in lung epithelial cells. In particular, we identified a regulatory link between Nkx2-1, the known tumor suppressor miR-200c, and the developmental and oncogenic transcription factors Nfib and Myb, adding new players to the regulatory mechanisms driven by Nkx2-1 in lung epithelial cells that may have implications in lung development and tumorigenesis. Keywords: microRNA Transcription factors Gene expression Lung epithelial cells Target

Genome-Wide Analyses of Nkx2-1 Binding to Transcriptional Target Genes Uncover Novel Regulatory Patterns Conserved in Lung Development and Tumors

The homeodomain transcription factor Nkx2-1 is essential for normal lung development and homeostasis. In lung tumors, it is considered a lineage survival oncogene and prognostic factor depending on its expression levels. The target genes directly bound by Nkx2-1, that could be the primary effectors of its functions in the different cellular contexts where it is expressed, are mostly unknown. In embryonic day 11.5 (E11.5) mouse lung, epithelial cells expressing Nkx2-1 are predominantly expanding, and in E19.5 prenatal lungs, Nkx2-1-expressing cells are predominantly differentiating in preparation for birth. To evaluate Nkx2-1 regulated networks in these two cell contexts, we analyzed genome-wide binding of Nkx2-1 to DNA regulatory regions by chromatin immunoprecipitation followed by tiling array analysis, and intersected these data to expression data sets. We further determined expression patterns of Nkx2-1 developmental target genes in human lung tumors and correlated their expression levels to that of endogenous NKX2-1. In these studies we uncovered differential Nkx2-1 regulated networks in early and late lung development, and a direct function of Nkx2-1 in regulation of the cell cycle by controlling the expression of proliferation-related genes. New targets, validated in Nkx2-1 shRNA transduced cell lines, include E2f3, Cyclin B1, Cyclin B2, and c-Met. Expression levels of Nkx2-1 direct target genes identified in mouse development significantly correlate or anti-correlate to the levels of endogenous NKX2-1 in a dosage-dependent manner in multiple human lung tumor expression data sets, supporting alternative roles for Nkx2-1 as a transcriptional activator or repressor, and direct regulator of cell cycle progression in development and tumors