Decomposing the Gender Wage Gap: The effect of firms, occupations and Job Stratification

This paper presents new evidence on the role of segregation into firms, occupations within a firm and stratification into professional categories within firm-occupations in explaining the gender wage gap. I use a generalized earnings model that allows observed and unobserved group characteristics to have different impact on wages of men and women within the same group. The database is a large sample of individual wage data from the 1995 Spanish Wage Structure Survey. Results indicate that firm segregation in our sample accounts for around one-fifth of the raw gender wage gap. Occupational segregation within firms accounts for about one-third of the raw wage gap, and stratification into different professional categories within firms and occupations explains another one-third of it. The remaining one-fifth of the overall gap arises from better outcomes of men relative to women within professional categories. It is also found that rewards to both observable and unobservable skills, particularly those related to education, are higher for males than for females within the same group. Finally, mean wages in occupations or job categories with a higher fraction of female co-workers are lower, but the negative impact of femaleness in higher for women.

Competitive Pressure and Job Interview Lying: A Game Theoretical Analysis

We consider a job contest in which candidates go through interviews (cheap talk) and are subject to reference checks. We show how competitive pressure - increasing the ratio of "good" to "bad" type candi- dates - can lead to a vast increase in lying and in some cases make bad hires more likely. As the number of candidates increases, it becomes harder to in- duce truth-telling. The interview stage becomes redundant if the candidates, a priori, know each others' type or the result of their own reference check. Finally, we show that the employer can bene t from committing not to reject all the applicants.

Autophagic Marker MAP1LC3B Expression Levels Are Associated with Carotid Atherosclerosis Symptomatology

Objectives: The mechanism by which atheroma plaque becomes unstable is not completely understood to date but analysis of differentially expressed genes in stable versus unstable plaques may provide clues. This will be crucial toward disclosing the mechanistic basis of plaque instability, and may help to identify prognostic biomarkers for ischaemic events. The objective of our study was to identify differences in expression levels of 59 selected genes between symptomatic patients (unstable plaques) and asymptomatic patients (stable plaques). Methods: 80 carotid plaques obtained by carotid endarterectomy and classified as symptomatic (>70% stenosis) or asymptomatic (>80% stenosis) were used in this study. The expression levels of 59 genes were quantified by qPCR on RNA extracted from the carotid plaques obtained by endarterectomy and analyzed by means of various bioinformatic tools. Results: Several genes associated with autophagy pathways displayed differential expression levels between asymptomatic and symptomatic (i.e. MAP1LC3B, RAB24, EVA1A). In particular, mRNA levels of MAP1LC3B, an autophagic marker, showed a 5-fold decrease in symptomatic samples, which was confirmed in protein blots. Immune system-related factors and endoplasmic reticulum-associated markers (i.e. ERP27, ITPR1, ERO1LB, TIMP1, IL12B) emerged as differently expressed genes between asymptomatic and symptomatic patients. Conclusions: Carotid atherosclerotic plaques in which MAP1LC3B is underexpressed would not be able to benefit from MAP1LC3B-associated autophagy. This may lead to accumulation of dead cells at lesion site with subsequent plaque destabilization leading to cerebrovascular events. Identified biomarkers and network interactions may represent novel targets for development of treatments against plaque destabilization and thus for the prevention of cerebrovascular events.