When Labour and Capital Collude: The Varieties of Welfare Capitalism and Early Retirement in Europe, Japan and the USA. CES Germany & Europe Working Papers, No. 00.4, 2000

The institutionalisation of early retirement has become a universal feature of postwar industrial economies, though there are significant cross-national variations. This paper studies the impact of different types of welfare regimes, production systems and labour relations on early exit from work. After an analysis of the main trends, the paper discusses the costs and benefits of early retirement for the various actors ��� labour, capital and the state ��� at different levels. The paper outlines both the "pull��� and "push��� factors of early exit. It first compares the distinct welfare state regimes and private occupational pensions in their impact on early retirement. Then it looks at the labour-shedding strategies inherent to particular employment regimes, production systems and financial governance structures. Finally, the impact of particular industrial relations systems, and especially the role of unions is discussed. The paper finds intricate "institutional complementarities��� between particular welfare states, production regimes and industrial relations systems, and these structure the incentives under which actors make decisions on work and retirement. The paper argues that the "collusion��� between capital, labour and the state in pursuing early retirement is not merely following a labour-shedding strategy to ease mass unemployment, but also caused by the need for economic restructuration, the downsizing pressures from financial markets, the maintenance of peaceful labour relations, and the consequences of a seniority employment system.

Expression at the Imprinted Dlk1-Gtl2 Locus Is Regulated by Proneural Genes in the Developing Telencephalon

Imprinting is an epigenetic mechanism that restrains the expression of about 100 genes to one allele depending on its parental origin. Several imprinted genes are implicated in neurodevelopmental brain disorders, such as autism, Angelman, and Prader-Willi syndromes. However, how expression of these imprinted genes is regulated during neural development is poorly understood. Here, using single and double KO animals for the transcription factors Neurogenin2 (Ngn2) and Achaete-scute homolog 1 (Ascl1), we found that the expression of a specific subset of imprinted genes is controlled by these proneural genes. Using in situ hybridization and quantitative PCR, we determined that five imprinted transcripts situated at the Dlk1-Gtl2 locus (Dlk1, Gtl2, Mirg, Rian, Rtl1) are upregulated in the dorsal telencephalon of Ngn2 KO mice. This suggests that Ngn2 influences the expression of the entire Dlk1-Gtl2 locus, independently of the parental origin of the transcripts. Interestingly 14 other imprinted genes situated at other imprinted loci were not affected by the loss of Ngn2. Finally, using Ngn2/Ascl1 double KO mice, we show that the upregulation of genes at the Dlk1-Gtl2 locus in Ngn2 KO animals requires a functional copy of Ascl1. Our data suggest a complex interplay between proneural genes in the developing forebrain that control the level of expression at the imprinted Dlk1-Gtl2 locus (but not of other imprinted genes). This raises the possibility that the transcripts of this selective locus participate in the biological effects of proneural genes in the developing telencephalon.

Evidence for two protein coding transcripts at the Igf2as locus

The insulin-like growth factor 2 antisense (Igf2as) gene is part of the Ins-Igf2-H19 imprinted gene cluster. The function of the paternally expressed Igf2as is still elusive. In our previous work, we showed that Igf2as transcripts were located in the cytoplasm of C2C12 mouse myoblast cells, associated with polysomes and polyadenylated suggesting that Igf2as is protein coding. In the present work, the protein coding capacity of Igf2as was investigated. We demonstrate for the first time the existence of a polypeptide translated from an Igf2as construct. Furthermore, an RNA-Seq analysis was performed using RNA prepared from skeletal muscles of newborn wild-type and ��� DMR1-U2 mice to further elucidate the function of Igf2as transcripts. We found no evidence for a regulatory role of Igf2as in the imprinted gene cluster. Interestingly, the RNA-Seq analysis indicated that Igf2as plays a role in the energy metabolism, the cell cycle, histone acetylation and muscle contraction pathways. Our Igf2as investigations further elucidated that there are two distinct Igf2as transcripts corresponding to two putative ORFs.

Genomic amplification of the caprine EDNRA locus might lead to a dose dependent loss of pigmentation

The South African Boer goat displays a characteristic white spotting phenotype, in which the pigment is limited to the head. Exploiting the existing phenotype variation within the breed, we mapped the locus causing this white spotting phenotype to chromosome 17 by genome wide association. Subsequent whole genome sequencing identified a 1���Mb copy number variant (CNV) harboring 5 genes including EDNRA. The analysis of 358 Boer goats revealed 3 alleles with one, two, and three copies of this CNV. The copy number is correlated with the degree of white spotting in goats. We propose a hypothesis that ectopic overexpression of a mutant EDNRA scavenges EDN3 required for EDNRB signaling and normal melanocyte development and thus likely lead to an absence of melanocytes in the non-pigmented body areas of Boer goats. Our findings demonstrate the value of domestic animals as reservoir of unique mutants and for identifying a precisely defined functional CNV.

Multiple regulatory variants located in cell type-specific enhancers within the PKP2 locus form major risk and protective haplotypes for canine atopic dermatitis in German shepherd dogs.

BACKGROUND Canine atopic dermatitis (CAD) is a chronic inflammatory skin disease triggered by allergic reactions involving IgE antibodies directed towards environmental allergens. We previously identified a ~1.5��Mb locus on canine chromosome 27 associated with CAD in German shepherd dogs (GSDs). Fine-mapping indicated association closest to the PKP2 gene encoding plakophilin 2. RESULTS Additional genotyping and association analyses in GSDs combined with control dogs from five breeds with low-risk for CAD revealed the top SNP 27:19,086,778 (p���=���1.4��������10(-7)) and a rare ~48��kb risk haplotype overlapping the PKP2 gene and shared only with other high-risk CAD breeds. We selected altogether nine SNPs (four top-associated in GSDs and five within the ~48��kb risk haplotype) that spanned ~280��kb forming one risk haplotype carried by 35��% of the GSD cases and 10��% of the GSD controls (OR���=���5.1, p���=���5.9��������10(-5)), and another haplotype present in 85��% of the GSD cases and 98��% of the GSD controls and conferring a protective effect against CAD in GSDs (OR���=���0.14, p���=���0.0032). Eight of these SNPs were analyzed for transcriptional regulation using reporter assays where all tested regions exerted regulatory effects on transcription in epithelial and/or immune cell lines, and seven SNPs showed allelic differences. The DNA fragment with the top-associated SNP 27:19,086,778 displayed the highest activity in keratinocytes with 11-fold induction of transcription by the risk allele versus 8-fold by the control allele (pdifference���=���0.003), and also mapped close (~3��kb) to an ENCODE skin-specific enhancer region. CONCLUSIONS Our experiments indicate that multiple CAD-associated genetic variants located in cell type-specific enhancers are involved in gene regulation in different cells and tissues. No single causative variant alone, but rather multiple variants combined in a risk haplotype likely contribute to an altered expression of the PKP2 gene, and possibly nearby genes, in immune and epithelial cells, and predispose GSDs to CAD.

El "An��lisis de Correspondencias M��ltiples" como herramienta metodol��gica de s��ntesis te��rica y emp��rica : Su aporte al estudio del locus universitario privado argentino (1955-1983)

El An��lisis de Correspondencias M��ltiples (ACM), recurso metodol��gico utilizado por Bourdieu y su equipo en un nivel avanzado de s��ntesis te��rico-emp��rica, constituye una herramienta fundamental para la construcci��n anal��tica de espacios relacionales. Permite posicionar relacionalmente unidades de an��lisis en funci��n de un conjunto determinado de variables y plasmar la multiplicidad resultante tanto gr��fica como anal��ticamente. Comenzando por una reflexi��n general sobre las potencialidades de la herramienta, este art��culo analiza la configuraci��n del espacio universitario privado en Argentina (1955-1983) a partir del ACM, que permiti�� determinar las relaciones de homolog��a y principios de diferenciaci��n existentes entre las instituciones que lo componen.

A manual of Gothic mouldings : a practical treatise on their formations, gradual development, combinations, and varieties /

Mode of access: Internet.

Characterization of tomato varieties and strains for constituents of fruit quality /

Cover title.

Abelian varieties.

Bibliography: p. 245-252.

Ducks and geese: standard varieties and management /

Omslagtitel.