Is there really a beauty premium or an ugliness penalty on earnings?

Purpose Economists have widely documented the “beauty premium” and “ugliness penalty” on earnings. Explanations based on employer and client discrimination would predict a monotonic association between physical attractiveness and earnings; explanations based on occupational self-selection would explain the beauty premium as a function of workers’ occupations; and explanations based on individual differences would predict that the beauty premium would disappear once appropriate individual differences are controlled. In this paper, we empirically tested the three competing hypotheses about the “beauty premium”. Design/Methodology/Approach We analyzed a nationally representative and prospectively longitudinal sample from the National Longitudinal Survey of Adolescent Health (Add Health). Findings Findings The results contradicted the discrimination and self-selection explanations and strongly supported the individual differences explanation. Very unattractive respondents always earned significantly more than unattractive respondents, sometimes more than average-looking or attractive respondents. Multiple regression analyses showed that there was very weak evidence for the beauty premium, and it disappeared completely once individual differences, such as health, intelligence, and Big Five personality factors, were statistically controlled. Implications Past findings of beauty premium and ugliness penalty may possibly be due to the fact that: 1) “very unattractive” and “unattractive” categories are usually collapsed into “below average” category; and 2) health, intelligence (as opposed to education) and Big Five personality factors are not controlled. It appears that more beautiful workers earn more, not because they are beautiful, but because they are healthier, more intelligent, and have better (more Conscientious and Extraverted, and less Neurotic) personality. Originality/Value This is the first study to show that: 1) very unattractive workers have extremely high earnings and earn more than physically more attractive workers, suggesting evidence for the potential ugliness premium; and 2) the apparent beauty premium and ugliness penalty may be a function of unmeasured traits correlated with physical attractiveness, such as health, intelligence, and personality

Integration of P2Y receptor-activated signal transduction pathways in G protein-dependent signalling networks

The role of nucleotides in intracellular energy provision and nucleic acid synthesis has been known for a long time. In the past decade, evidence has been presented that, in addition to these functions, nucleotides are also autocrine and paracrine messenger molecules that initiate and regulate a large number of biological processes. The actions of extracellular nucleotides are mediated by ionotropic P2X and metabotropic P2Y receptors, while hydrolysis by ecto-enzymes modulates the initial signal. An increasing number of studies have been performed to obtain information on the signal transduction pathways activated by nucleotide receptors. The development of specific and stable purinergic receptor agonists and antagonists with therapeutical potential largely contributed to the identification of receptors responsible for nucleotide-activated pathways. This article reviews the signal transduction pathways activated by P2Y receptors, the involved second messenger systems, GTPases and protein kinases, as well as recent findings concerning P2Y receptor signalling in C6 glioma cells. Besides vertical signal transduction, lateral cross-talks with pathways activated by other G protein-coupled receptors and growth factor receptors are discussed

Cross talk between the Akt and p38α pathways in macrophages downstream of Toll-like receptor signaling.

The stimulation of Toll-like receptors (TLRs) on macrophages by pathogen-associated molecular patterns (PAMPs) results in the activation of intracellular signaling pathways that are required for initiating a host immune response. Both phosphatidylinositol 3-kinase (PI3K)-Akt and p38 mitogen-activated protein kinase (MAPK) signaling pathways are activated rapidly in response to TLR activation and are required to coordinate effective host responses to pathogen invasion. In this study, we analyzed the role of the p38-dependent kinases MK2/3 in the activation of Akt and show that lipopolysaccharide (LPS)-induced phosphorylation of Akt on Thr308 and Ser473 requires p38α and MK2/3. In cells treated with p38 inhibitors or an MK2/3 inhibitor, phosphorylation of Akt on Ser473 and Thr308 is reduced and Akt activity is inhibited. Furthermore, BMDMs deficient in MK2/3 display greatly reduced phosphorylation of Ser473 and Thr308 following TLR stimulation. However, MK2/3 do not directly phosphorylate Akt in macrophages but act upstream of PDK1 and mTORC2 to regulate Akt phosphorylation. Akt is recruited to phosphatidylinositol 3,4,5-trisphosphate (PIP3) in the membrane, where it is activated by PDK1 and mTORC2. Analysis of lipid levels in MK2/3-deficient bone marrow-derived macrophages (BMDMs) revealed a role for MK2/3 in regulating Akt activity by affecting availability of PIP3 at the membrane. These data describe a novel role for p38α-MK2/3 in regulating TLR-induced Akt activation in macrophages

Structural insights into the regulation of PDK1 by phosphoinositides and inositol phosphates

3-phosphoinositide-dependent protein kinase-1 (PDK1) phosphorylates and activates many kinases belonging to the AGC subfamily. PDK1 possesses a C-terminal pleckstrin homology (PH) domain that interacts with PtdIns(3,4,5)P(3)/PtdIns(3,4)P(2) and with lower affinity to PtdIns(4,5)P(2). We describe the crystal structure of the PDK1 PH domain, in the absence and presence of PtdIns(3,4,5)P(3) and Ins(1,3,4,5)P(4). The structures reveal a ‘budded' PH domain fold, possessing an N-terminal extension forming an integral part of the overall fold, and display an unusually spacious ligand-binding site. Mutagenesis and lipid-binding studies were used to define the contribution of residues involved in phosphoinositide binding. Using a novel quantitative binding assay, we found that Ins(1,3,4,5,6)P(5) and InsP(6), which are present at micromolar levels in the cytosol, interact with full-length PDK1 with nanomolar affinities. Utilising the isolated PDK1 PH domain, which has reduced affinity for Ins(1,3,4,5,6)P(5)/InsP(6), we perform localisation studies that suggest that these inositol phosphates serve to anchor a portion of cellular PDK1 in the cytosol, where it could activate its substrates such as p70 S6-kinase and p90 ribosomal S6 kinase that do not interact with phosphoinositides

Loss of PTEN selectively desensitizes upstream IGF1 and insulin signaling

Many tumours have chronically elevated activity of PI 3-kinase dependent signalling pathways, caused largely by oncogenic mutation of PI 3-kinase itself or loss of the opposing tumour suppressor lipid phosphatase, PTEN. Several PI 3-kinase dependent feedback mechanisms have been identified that may affect the sensitivity of upstream receptor signalling, but the events required to initiate an inhibited state have not been addressed. We show that in a variety of cell types, loss of PTEN via experimental knockdown or in tumour cell lines correlates with a block in IGF1/insulin signalling, without affecting the sensitivity of PDGF or EGF signalling. These effects on IGF/insulin signalling include a reduction of up to five to ten fold in IGF stimulated PI 3-kinase activation, a failure to activate the ERK kinases, and in some cells, reduced expression of IRS1, and both IGF1 and insulin receptors. These data indicate that chronically elevated PI 3-kinase dependent signalling to the degree seen in many tumours causes a selective loss of sensitivity in IGF1/insulin signalling that could significantly reduce the selective advantage of deregulated activation of IGF1/IGF1-R signalling in tumour development

Early processing of emotional faces in a Go/NoGo task: lack of N170 right-hemispheric specialisation in children with major depression

Emotionally biased information processing towards sad and away from happy information characterises individuals with major depression. To learn more about the nature of these dysfunctional modulations, developmental and neural aspects of emotional face processing have to be considered. By combining measures of performance (attention control, inhibition) in an emotional Go/NoGo task with an event-related potential (ERP) of early face processing (N170), we obtained a multifaceted picture of emotional face processing in a sample of children and adolescents (11-14 years) with major depression (MDD, n = 26) and healthy controls (CTRL, n = 26). Subjects had to respond to emotional faces (fearful, happy or sad) and withhold their response to calm faces or vice versa. Children of the MDD group displayed shorter N170 latencies than children of the CTRL group. Typical right lateralisation of the N170 was observed for all faces in the CTRL but not for happy and calm faces in the MDD group. However, the MDD group did not differ in their behavioural reaction to emotional faces, and effects of interference by emotional information on the reaction to calm faces in this group were notably mild. Although we could not find a typical pattern of emotional bias, the results suggest that alterations in face processing of children with major depression can be seen at early stages of face perception indexed by the N170. The findings call for longitudinal examinations considering effects of development in children with major depression as well as associations to later stages of processing