Why would some migrants choose to engage in degrading work?

This paper develops a model of voluntary migration into degrading work. The essence of the model is a tension between two “bads:” that which arises from being relatively deprived at home, and that which arises from engaging in humiliating work away from home. Balancing between these two “bads” can give rise to an explicit, voluntary choice to engage in humiliating work. The paper identifies conditions under which a migrant will choose to engage in degrading work rather than being forced into it, to work abroad as a prostitute, say, rather than on a farm. The paper delineates the possible equilibria and finds that greater relative deprivation will make it more likely that the equilibrium outcome will be “engagement in prostitution.” It is shown that under well specified conditions, every individual will work as a prostitute, yet every individual would be better off working on a farm. Put differently, when specific conditions are satisfied, there is a possibility of a “coordination failure:” if individuals believe that everyone else will choose to be a prostitute, this belief will be self-fulfilling. In this case, all the individuals choose to engage in prostitution, which renders each of them worse off. The paper discusses various policy implications. It is shown that a policy intervention (a crackdown on migrants’ engagement in prostitution), if implemented strictly, can increase everyone’s welfare, but when the policy is implemented loosely, cracking down on prostitution will only reduce individuals’ welfare without reducing their engagement in prostitution.Migrants, Relative deprivation, Degrading work, Humiliation, Multiple equilibria, Welfare assessment, Policy implications, Labor and Human Capital, Political Economy, F22, J24, J81,

Dishevelled regulates the metabolism of amyloid precursor protein via protein kinase C/Mitogen-activated protein kinase and c-Jun terminal kinase

Alzheimer’s disease (AD) is a disorder of two pathologies: amyloid plaques, the core of which is a peptide derived from the amyloid precursor protein (APP), and neurofibrillary tangles composed of highly phosphorylated tau. Protein kinase C (PKC)is known to increase non-amyloidogenic a-secretase cleavage of APP, producing secreted APP (sAPPa), and glycogen synthasekinase (GSK)-3b is known to increase tau phosphorylation. Both PKC and GSK-3b are components of the wnt signaling cascade. Here we demonstrate that overexpression of another member of this pathway, dishevelled (dvl-1), increasess APPa production. The dishevelled action on APP is mediated via both c-jun terminal kinase (JNK) and protein kinase C(PKC)/mitogen-activated protein (MAP) kinase but not via p38MAP kinase. These data position dvl-1 upstream of both PKCand JNK, thereby explaining the previously observed dual signaling action of dvl-1. Furthermore, we show that human dvl-1and wnt-1 also reduce the phosphorylation of tau by GSK-3b. Therefore, both APP metabolism and tau phosphorylation are potentially linked through wnt signaling

Human epithelial model systems for the study of Candida infections in vitro. Pt.II: Histologic methods for studying fungal invasion

Although the role of invasion in the virulence of Candida albicans has been demonstrated, the mechanism that governs fungal invasion is not fully understood. Among the tools that exist to fill these gaps in knowledge, in vitro tissue models based on reconstituted human epithelia (RHE) have already been developed. Such models are designed to study more reproducably the fungus-host relationship, as they eliminate the complexity and variability found in vivo. Herein we describe the preparation of these RHE and their application in study of the invasion properties of C. albicans by further histologic processing and microscopic observation. For this purpose, different epithelial cell lines are grown on a collagen gel to build up models of intestinal (Caco-2 cell line), vaginal (A431 cell line), and oral (TR146 cell line) mucosa. The use of these in vitro models applied to test the invasiveness of C. albicans strains (clinical isolates or gene deleted mutants) and to identify changes in gene expression during the invasion of the RHE will help to advance our knowledge of pathogenesis and to study specific mechanisms used by C. albicans to adapt to changing environments present in different epithelia. Furthermore, because these models are useful to study the host response during the challenge with the pathogen, they will also offer important new insights into host cell biology and identify new targets for treatment