Essays on Wage Inequality and Poverty

This thesis sets out to study the impact of growth and technological development on inequality. This thesis focuses on two types of inequality, the skill premium (wage inequality between skilled and unskilled labour) and the poverty. First, this thesis sets out to analyze the interaction between the skill premium and the growth and development in England in the very long run (circa 1329-1660); Second, it studies the poverty-reduction effect of the interaction between institutional development and remittances. These two topics are covered by Chapters 2, 3 and 4 respectively. Chapter 2 studies the evolution of the skill premium in England from 1329 to 1660. It develops a unified model that accounts for the growth and development in the historical period that ranging from late medieval ear to industrial revolution. This model unveils insightful linkage between the historical development in this period and the skill premium. It shows that the growth of the relative abundance of physical capital to human capital from an initally low level to a sufficiently high level, which is triggered by demographic change and the growth of agricultural productivity, brings about the decline of the skill premiumfrom1329 to 1450s, and the stabilization of the skill premiumafterwards. On the basis of the analytical findings in Chapter 2, Chapter 3 brings the proposed unified model of growth into data. Through calibration and simulation, it shows that the with the simulated skill premium declining to a low and stable level, the simulated GDP per capita grows to a high and stable level and the simulated primary sector labour share declines from a high level at the beginning to a low level in the end, both of which are consistent with the actual data. The simulated skill premium, GDP per capita and the primary sector labour share jointly show the gradual ‘modernization” of the English economy takes place well before the industrial revolution. Chapter 4 analyzes the impact of institutional development of the povertyreduction effect of remittances. Considering remittances and remittances’ facilitating effect on financial development, it shows that institutional development attract more remittances. This then reduces credit market imperfection and enables a larger fraction of the population to invest in human capital and escape poverty trap, which results in the reduction of poverty. This chapter is the first to analytically study the change in poverty in response to remittances and institutional development

Gene ontology enrichment of the Pink module.

<p>Gene ontology of each module was analyzed using the DAVID function analysis tool. The pink module was enriched with many categories of genes that are involved in synaptic plasticity.</p

Correlation of nicotine intake with gene expression measured by PCR in AcbS.

<p>A total of 13 genes were selected for validation. The levels of gene expression obtained by RNAseq vs. real-time PCR were correlated with the amount of nicotine intake from the same strains (data reported previously <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0086214#pone.0086214-Chen3" target="_blank">[29]</a>).</p

Genes of modules correlated with nicotine intake that were implicated in smoking behavior.

<p>A literature mining software, Chilibot <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0086214#pone.0086214-Chen5" target="_blank">[48]</a>, was used to search for genes reported to be involved in smoking behavior. Manually curated results confirmed that 15 genes of the Pink module were potentially associated with smoking behaviors. Searching 2 additional modules with similar numbers of genes found only 1 gene potentially associated with smoking behavior.</p

Nnat of the Pink module.

<p>The eigenvalue of the Pink module was significantly correlated with nicotine intake (A) but its correlation with food reward earned was not significant (B), suggesting behavioral specificity of the module. Nnat contributed strongly to the expression characteristics of the Pink module (C). The expression pattern of Nnat across the 10 strains measured by PCR showed significant correlation with nicotine intake (D). Strains: BN: Brown Norway, DA: Dark Agouti, F344: Fisher 344, Lew: Lewis, SHR: Spontaneous hypertensive rat, WKY: Wistar-Kyoto. For the F1 hybrids, the two letters representing the initials of the maternal and paternal strains were used.</p

WGCNA detected networks of correlated genes.

<p>(A) Weighted Gene Correlation Network Analysis (WGCNA) was applied to 12,639 genes. A total of 127 modules were identified in AcbS. Each module was named after a unique color assigned by the algorithm. Genes within each module were strongly correlated with each other across all the samples. (B) Modules significantly associated with any of the listed traits are plotted. Twelve modules were associated with stable levels of nicotine intake during last 3 d of SA (when nicotine intakes were stable). Of the 12 modules, nine were negatively correlated with nicotine intake, suggesting their expression in the AcbS protect against voluntary nicotine intake in adolescent rodents.</p

Validation of transcriptome sequencing data using real-time PCR.

<p>A total of 13 genes were selected based on the following: strong correlation with the module or nicotine intake; high module membership; strong connectivity within the module. Validation by real-time PCR was conducted using another set of AcbS samples obtained from the same rat strains. The level of gene expression, assayed by transcriptome sequencing vs. PCR across the 10 strains, showed strong correlation (rho  = 0.76 p<0.001).</p

Label-Free Quantitative Phosphoproteomic Analysis Reveals Differentially Regulated Proteins and Pathway in PRRSV-Infected Pulmonary Alveolar Macrophages

Porcine reproductive and respiratory syndrome virus (PRRSV) is an important pathogen of swine worldwide and causes significant economic losses. Through regulating the host proteins phosphorylation, PRRSV was found to manipulate the activities of several signaling molecules to regulate innate immune responses. However, the role of protein phosphorylation during PRRSV infection and the signal pathways responsible for it are relatively unknown. Here liquid chromatography–tandem mass spectrometry for label-free quantitative phosphoproteomics was applied to systematically investigate the global phosphorylation events in PRRSV-infected pulmonary alveolar macrophages. In total, we identified 2125 unique phosphosites, of which the phosphorylation level of 292 phosphosites on 242 proteins and 373 phosphosites on 249 proteins was significantly altered at 12 and 36 h pi, respectively. The phosphoproteomics data were analyzed using ingenuity pathways analysis to identify defined canonical pathways and functional networks. Pathway analysis revealed that PRRSV-induced inflammatory cytokines production was probably due to the activation of mitogen-activated protein kinase and NF-κB signal pathway, which were regulated by several protein kinases during virus infection. Interacting network analysis indicated that altered phosphoproteins were involved in cellular assembly and organization, protein synthesis, molecular transport, and signal transduction in PRRSV infected cells. These pathways and functional networks analysis could provide direct insights into the biological significance of phosphorylation events modulated by PRRSV and may help us elucidate the pathogenic mechanisms of PRRSV infection

Quantitative Proteomic Analysis Reveals That Transmissible Gastroenteritis Virus Activates the JAK-STAT1 Signaling Pathway

Transmissible gastroenteritis virus (TGEV), a porcine enteropathogenic coronavirus, causes lethal watery diarrhea and severe dehydration in piglets. In this study, liquid chromatography–tandem mass spectrometry coupled to isobaric tags for relative and absolute quantification labeling was used to quantitatively identify differentially expressed cellular proteins after TGEV infection in PK-15 cells. In total, 162 differentially expressed cellular proteins were identified, including 60 upregulated proteins and 102 downregulated proteins. These differentially expressed proteins were involved in the cell cycle, cellular growth and proliferation, the innate immune response, etc. Interestingly, many upregulated proteins were associated with interferon signaling, especially signal transducer and activator of transcription 1 (STAT1) and interferon-stimulated genes (ISGs). Immunoblotting and real-time quantitative reverse transcription polymerase chain reaction demonstrated that TGEV infection induces STAT1 phosphorylation and nuclear translocation, as well as ISG expression. This study for the first time reveals that TGEV induces interferon signaling from the point of proteomic analysis

Label-Free Quantitative Phosphoproteomic Analysis Reveals Differentially Regulated Proteins and Pathway in PRRSV-Infected Pulmonary Alveolar Macrophages

Porcine reproductive and respiratory syndrome virus (PRRSV) is an important pathogen of swine worldwide and causes significant economic losses. Through regulating the host proteins phosphorylation, PRRSV was found to manipulate the activities of several signaling molecules to regulate innate immune responses. However, the role of protein phosphorylation during PRRSV infection and the signal pathways responsible for it are relatively unknown. Here liquid chromatography–tandem mass spectrometry for label-free quantitative phosphoproteomics was applied to systematically investigate the global phosphorylation events in PRRSV-infected pulmonary alveolar macrophages. In total, we identified 2125 unique phosphosites, of which the phosphorylation level of 292 phosphosites on 242 proteins and 373 phosphosites on 249 proteins was significantly altered at 12 and 36 h pi, respectively. The phosphoproteomics data were analyzed using ingenuity pathways analysis to identify defined canonical pathways and functional networks. Pathway analysis revealed that PRRSV-induced inflammatory cytokines production was probably due to the activation of mitogen-activated protein kinase and NF-κB signal pathway, which were regulated by several protein kinases during virus infection. Interacting network analysis indicated that altered phosphoproteins were involved in cellular assembly and organization, protein synthesis, molecular transport, and signal transduction in PRRSV infected cells. These pathways and functional networks analysis could provide direct insights into the biological significance of phosphorylation events modulated by PRRSV and may help us elucidate the pathogenic mechanisms of PRRSV infection