110 research outputs found

    Explaining Gender Differences in Unemployment with Micro Data on Flows in Post-Communist Economies

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    Post-communist labor markets provide an interesting laboratory since unemployment rates grew from zero to double digits and gender differences began to vary greatly across these countries. We provide the first systematic analysis of the determinants of the gender unemployment gap in the Czech Republic using a method that decomposes unemployment rates into transition probabilities (flows) between labor market states, which we calculate using Labor Force Survey data. We extend the analysis to other post-communist economies by evaluating the flows available from existing studies with the decomposition framework. We further examine the flows in the Czech Republic by estimating gender-specific multinomial logit models to learn which factors (demographic, regional, cyclical) other than gender and marital status affect unemployment. We find that women’s lower probability of exiting unemployment for a job explains the lion’s share of the gender gap in the unemployment rates in the Czech Republic and the other post-communist countries for which studies exist. This is also the principal factor explaining married women’s higher unemployment rates compared to married men in the Czech Republic. On the other hand, single men and women’s rates are higher than married men and women’s because they are twice as likely to lose/leave a job for unemployment. We find that age and education are systematically important in explaining flows of both men and women in all these economies, as it is in the more developed industrial economies. The less educated are more likely to be laid off or quit and less likely to find a job. Whereas younger individuals are more likely to be laid off or quit, they are also more likely to find a job.http://deepblue.lib.umich.edu/bitstream/2027.42/39891/3/wp506.pd

    Explaining Gender Differences in Unemployment with Micro Data on Flows in Post-Communist Economies

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    Post-communist labor markets provide an interesting laboratory since unemployment rates grew from zero to double digits and gender differences began to vary greatly across these countries. We provide the first systematic analysis of the determinants of the gender unemployment gap in the Czech Republic using a method that decomposes unemployment rates into transition probabilities (flows) between labor market states, which we calculate using Labor Force Survey data. We extend the analysis to other post-communist economies by evaluating the flows available from existing studies with the decomposition framework. We further examine the flows in the Czech Republic by estimating gender-specific multinomial logit models to learn which factors (demographic, regional, cyclical) other than gender and marital status affect unemployment. We find that women’s lower probability of exiting unemployment for a job explains the lion’s share of the gender gap in the unemployment rates in the Czech Republic and the other post-communist countries for which studies exist. This is also the principal factor explaining married women’s higher unemployment rates compared to married men in the Czech Republic. On the other hand, single men and women’s rates are higher than married men and women’s because they are twice as likely to lose/leave a job for unemployment. We find that age and education are systematically important in explaining flows of both men and women in all these economies, as it is in the more developed industrial economies. The less educated are more likely to be laid off or quit and less likely to find a job. Whereas younger individuals are more likely to be laid off or quit, they are also more likely to find a job.Unemployment, Gender, Transition Probabilities, Flow Analysis, Post-communist economies, Czech Republic

    Clinical evaluation of spasticity and feasibility of its interference

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    Department of RehabilitationRehabilitačnĂ­ klinikaFaculty of Medicine in Hradec KrĂĄlovĂ©LĂ©kaƙskĂĄ fakulta v Hradci KrĂĄlov

    Localizing order to boost signaling

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    CCR6 is expressed on an IL-10–producing, autoreactive memory T cell population with context-dependent regulatory function

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    Interleukin (IL)-10 produced by regulatory T cell subsets is important for the prevention of autoimmunity and immunopathology, but little is known about the phenotype and function of IL-10–producing memory T cells. Human CD4+CCR6+ memory T cells contained comparable numbers of IL-17– and IL-10–producing cells, and CCR6 was induced under both Th17-promoting conditions and upon tolerogenic T cell priming with transforming growth factor (TGF)–ÎČ. In normal human spleens, the majority of CCR6+ memory T cells were in the close vicinity of CCR6+ myeloid dendritic cells (mDCs), and strikingly, some of them were secreting IL-10 in situ. Furthermore, CCR6+ memory T cells produced suppressive IL-10 but not IL-2 upon stimulation with autologous immature mDCs ex vivo, and secreted IL-10 efficiently in response to suboptimal T cell receptor (TCR) stimulation with anti-CD3 antibodies. However, optimal TCR stimulation of CCR6+ T cells induced expression of IL-2, interferon-Îł, CCL20, and CD40L, and autoreactive CCR6+ T cell lines responded to various recall antigens. Notably, we isolated autoreactive CCR6+ T cell clones with context-dependent behavior that produced IL-10 with autologous mDCs alone, but that secreted IL-2 and proliferated upon stimulation with tetanus toxoid. We propose the novel concept that a population of memory T cells, which is fully equipped to participate in secondary immune responses upon recognition of a relevant recall antigen, contributes to the maintenance of tolerance under steady-state conditions

    TCR ligand density and affinity determine peripheral induction of Foxp3 in vivo

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    T cell receptor (TCR) ligation is required for the extrathymic differentiation of forkhead box p3+ (Foxp3+) regulatory T cells. Several lines of evidence indicate that weak TCR stimulation favors induction of Foxp3 in the periphery; however, it remains to be determined how TCR ligand potency influences this process. We characterized the density and affinity of TCR ligand favorable for Foxp3 induction and found that a low dose of a strong agonist resulted in maximal induction of Foxp3 in vivo. Initial Foxp3 induction by weak agonist peptide could be enhanced by disruption of TCR–peptide major histocompatibility complex (pMHC) interactions or alteration of peptide dose. However, time course experiments revealed that Foxp3-positive cells induced by weak agonist stimulation are deleted, along with their Foxp3-negative counterparts, whereas Foxp3-positive cells induced by low doses of the strong agonist persist. Our results suggest that, together, pMHC ligand potency, density, and duration of TCR interactions define a cumulative quantity of TCR stimulation that determines initial peripheral Foxp3 induction. However, in the persistence of induced Foxp3+ T cells, TCR ligand potency and density are noninterchangeable factors that influence the route to peripheral tolerance

    Self–class I MHC molecules support survival of naive CD8 T cells, but depress their functional sensitivity through regulation of CD8 expression levels

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    Previous studies have suggested that naive CD8 T cells require self-peptide–major histocompatability complex (MHC) complexes for maintenance. However, interpretation of such studies is complicated because of the involvement of lymphopenic animals, as lymphopenia drastically alters naive T cell homeostasis and function. In this study, we explored naive CD8 T cell survival and function in nonlymphopenic conditions by using bone marrow chimeric donors and hosts in which class I MHC expression is absent or limited to radiosensitive versus radioresistant cells. We found that long-term survival of naive CD8 T cells (but not CD4 T cells) was impaired in the absence of class I MHC. However, distinct from this effect, class I MHC deprivation also enhanced naive CD8 T cell responsiveness to low-affinity (but not high-affinity) peptide–MHC ligands. We found that this improved sensitivity was a consequence of up-regulated CD8 levels, which was mediated through a transcriptional mechanism. Hence, our data suggest that, in a nonlymphopenic setting, self-class I MHC molecules support CD8 T cell survival, but that these interactions also attenuate naive T cell sensitivity by dynamic tuning of CD8 levels
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