Essays in Family Economics

This dissertation consists of three essays in family economics. The underlying objective of this dissertation is to better understand inequality in family formation and in intra-household allocation. The first two chapters study racial sorting in the United States marriage market. The third chapter studies the effects of higher female bargaining power on household consumption of married couples in the United States. Chapter 1 studies the unequal gains from racial desegregation in the United States marriage market. Interracial marriages have increased in the United States over the past several decades, but the trends differ across race, gender, and education groups. This suggests that racial desegregation in the marriage market may not have equally improved the marriage prospects of different groups. This paper studies why some groups have gained more from marital desegregation than others over the past four decades. To this end, I build a transferable utility matching model to define and estimate the welfare gains from marital desegregation by comparing the equilibrium rates of singlehood in the observed marriage market with those in a completely segregated marriage market. I find that among Blacks and Whites, college-educated men gained more than their female and lower-educated male counterparts. To understand why, I implement a decomposition method to quantify how changing population and changing marital surplus have shaped the unequal gains, accounting for general equilibrium effects. I find that the rise in the welfare gains for college-educated Black men is largely driven by the increase in the joint surplus from marriage with college-educated White women. Other Black men and women did not benefit as much from any change in the marital surplus, implying that race relations have not substantially improved in the marriage market except for the most educated Black men. I also find that the rise in welfare gains for college-educated White men is driven by the female-biased population increase among college graduates. Simulation results suggest that fixing the unbalance in marital surplus and making progress toward racial integration in the marriage market would significantly improve marriage outcomes for Black men and women. Chapter 2 examines the geographical variation in racial sorting in the United States marriage market. There are substantial variations in interracial marriage rates across states, but it is challenging to disentangle the role of marital surplus from the population composition. I use a structural marriage market model to document the geographical variation and time trends in the racial assortativeness in marital matching across the US states. I document several new facts. First, preference for same-race marriage compared to different-race marriage is the highest in the southern states and the lowest in the western states, even after controlling for the demographic composition. Second, the ranking of each state in terms of racial assortative matching has been persistent over the past four decades. Third, the geographic variation in racial assortative matching is closely related to the racial attitudes of White respondents, but not of Black respondents. This suggests that geographic variation in racial assortative matching may be driven more by White people's marital preferences than by Black people's marital preferences. In terms of individual welfare gains from interracial marriage, I find that higher-educated Black men living in the West benefit more from interracial marriage and those living in the South do not benefit at all from interracial marriage. This is consistent with the geographical patterns in racial assortative matching. On the other hand, Black women do not benefit at all from interracial marriage regardless of where they live. Chapter 3, which is joint work with So Yoon Ahn, studies how spousal bargaining power affects consumption patterns of married households in the US, using a detailed barcode-level dataset. While there has been substantial evidence from developing countries settings that bargaining power within the household affects household consumption, there is a lack of such evidence in more developed country settings like the US. To study this, we use two distribution factors as proxies for spousal bargaining power: spouses' relative education and spouses' relative potential wage, which is our preferred distribution factor. As an arguably exogenous measure of bargaining power, our relative potential wage is constructed as a Bartik-style measure of the female-to-male wage ratio, exploiting county-level variations in heterogeneous exposure to different industries and state-wide wage growth. We find that the expenditure shares on women's beauty goods increase and the expenditure shares on alcohol decrease significantly both when the relative education of wives increases and when the relative potential wages of wives increase. These results are consistent with household bargaining explanations. For couples with children, improved women's household bargaining position is associated with a higher budget share on books, stationery, and school supplies, which are potentially related to investment in children. Our evidence shows that local labor market condition that is favorable to women than men shifts household consumption towards more female-preferred goods among married couples in the US

Evaluation of the Reggio approach to early education

We evaluate the Reggio Approach using non-experimental data on individuals from the cities of Reggio Emilia, Parma and Padova belonging to one of five age cohorts: ages 50, 40, 30, 18, and 6 as of 2012. The treated were exposed to municipally offered infant-toddler (ages 0–3) and preschool (ages 3–6) programs in Reggio Emilia. The control group either did not receive formal childcare or were exposed to programs offered by municipal systems (outside of Reggio Emilia), or by state or religious systems (in all three cities). We exploit the city-cohort structure of the data to estimate treatment effects using three strategies: difference-in-differences, matching, and matched-difference-in-differences. Most positive and significant effects are generated from comparisons of the treated with individuals who did not receive formal childcare. Relative to not receiving formal care, the Reggio Approach significantly boosts outcomes related to employment, socio-emotional skills, high school graduation, participation in elections, and obesity. Comparisons with individuals exposed to alternative forms of childcare do not yield strong patterns of positive and significant effects. This suggests that differences between the Reggio Approach and other alternatives are not sufficiently large to result in significant differences in outcomes. This interpretation is supported by a survey we conduct, which documents increasing similarities in the administrative and pedagogical practices of childcare systems in the three cities over time

Evaluation of the Reggio approach to early education

We evaluate the Reggio Approach using non-experimental data on individuals from the cities of Reggio Emilia, Parma and Padova belonging to one of five age cohorts: ages 50, 40, 30, 18, and 6 as of 2012. The treated were exposed to municipally offered infant-toddler (ages 0–3) and preschool (ages 3–6) programs in Reggio Emilia. The control group either did not receive formal childcare or were exposed to programs offered by municipal systems (outside of Reggio Emilia), or by state or religious systems (in all three cities). We exploit the city-cohort structure of the data to estimate treatment effects using three strategies: difference-in-differences, matching, and matched-difference-in-differences. Most positive and significant effects are generated from comparisons of the treated with individuals who did not receive formal childcare. Relative to not receiving formal care, the Reggio Approach significantly boosts outcomes related to employment, socio-emotional skills, high school graduation, participation in elections, and obesity. Comparisons with individuals exposed to alternative forms of childcare do not yield strong patterns of positive and significant effects. This suggests that differences between the Reggio Approach and other alternatives are not sufficiently large to result in significant differences in outcomes. This interpretation is supported by a survey we conduct, which documents increasing similarities in the administrative and pedagogical practices of childcare systems in the three cities over time

Diagnosis and Treatment of Nontuberculous Mycobacterial Pulmonary Diseases: A Korean Perspective

The incidence of pulmonary disease caused by nontuberculous mycobacteria (NTM) appears to be increasing worldwide. In Korea, M. avium complex and M. abscessus account for most of the pathogens encountered, whilst M. kansasii is a relatively uncommon cause of NTM pulmonary diseases. NTM pulmonary disease is highly complex in terms of its clinical presentation and management. Because its clinical features are indistinguishable from those of pulmonary tuberculosis and NTMs are ubiquitous in the environment, the isolation and identification of causative organisms are mandatory for diagnosis, and some specific diagnostic criteria have been proposed. The treatment of NTM pulmonary disease depends on the infecting species, but decisions concerning the institution of treatment are never easy. Treatment requires the use of multiple drugs for 18 to 24 months. Thus, treatment is expensive, often has significant side effects, and is frequently not curative. Therefore, clinicians should be confident that there is sufficient pathology to warrant prolonged, multidrug treatment regimens. In all of the situations, outcomes can be best optimized only when clinicians, radiologists, and laboratories work cooperatively

Expression and regulation of Enpp2 in rat uterus during the estrous cycle

Ectonucleotide pyrophosphatase/phosphodiestrase 2 (Enpp2) isolated from the supernatant of human melanoma cells is a lysophospholipase D that transforms lysophosphatidylcholine into lysophospatidic acid. Although multiple analyses have investigated the function of Enpp2 in the hypothalamus, its role in the uterus during the estrous cycle is not well understood. In the present study, rat uterine Enpp2 was analyzed by RT-PCR, Western blotting, and immunohistochemistry. Quantitative PCR analysis demonstrated that uterine Enpp2 mRNA was decreased during estrus compared to proestrus and diestrus. To determine whether uterine Enpp2 expression is affected by sex steroid hormones, immature rats were treated with 17β-estradiol (E2), progesterone, or both on postnatal days 14 to 16. Interestingly, the expression of Enpp2 mRNA and protein were down-regulated by E2 in the uterus during estrus but not during proestrus or diestrus, suggesting that Enpp2 may play a role in uterine function during estrus. Enpp2 is primarily localized in the stromal cells of the endometrium during proestrus and estrus. During diestrus, Enpp2 was highly expressed in the epithelial cells of the endometrium. Taken together, these results suggest that uterine Enpp2 may be regulated by E2 and plays a role in reproductive functions during female rat development

Discovery of a Novel hsp65 Genotype within Mycobacterium massiliense Associated with the Rough Colony Morphology

So far, genetic diversity among strains within Mycobacterium massiliense has rarely been studied. To investigate the genetic diversity among M. massiliense, we conducted phylogenetic analysis based on hsp65 (603-bp) and rpoB (711-bp) sequences from 65 M. massiliense Korean isolates. We found that hsp65 sequence analysis could clearly differentiate them into two distinct genotypes, Type I and Type II, which were isolated from 35 (53.8%) and 30 patients (46.2%), respectively. The rpoB sequence analysis revealed a total of four genotypes (R-I to R-IV) within M. massiliense strains, three of which (R-I, R-II and R-III) correlated with hsp65 Type I, and other (R-IV), which correlated with Type II. Interestingly, genotyping by the hsp65 method agreed well with colony morphology. Despite some exceptions, Type I and II correlated with smooth and rough colonies, respectively. Also, both types were completely different from one another in terms of MALDI-TOF mass spectrometry profiles of whole lipid. In addition, we developed PCR-restriction analysis (PRA) based on the Hinf I digestion of 644-bp hsp65 PCR amplicons, which enables the two genotypes within M. massiliense to be easily and reliably separated. In conclusion, two distinct hsp65 genotypes exist within M. massiliense strains, which differ from one another in terms of both morphology and lipid profile. Furthermore, our data indicates that Type II is a novel M. massiliense genotype being herein presented for the first time. The disparity in clinical traits between these two hsp65 genotypes needs to be exploited in the future study

Efficacy and Safety of Evogliptin Add-on Therapy to Dapagliflozin/Metformin Combinations in Patients with Poorly Controlled Type 2 Diabetes Mellitus: A 24-Week Multicenter Randomized Placebo-Controlled Parallel-Design Phase-3 Trial with a 28-Week Extension

Background This study investigates the long-term efficacy and safety of evogliptin add-on therapy in patients with inadequately controlled type 2 diabetes mellitus (T2DM) previously received dapagliflozin and metformin (DAPA/MET) combination. Methods In this multicenter randomized placebo-controlled phase 3 trial, patients with glycosylated hemoglobin (HbA1c) levels 7.0% to 10.5% (n=283) previously used DAPA 10 mg plus MET (≥1,000 mg) were randomly assigned to the evogliptin 5 mg once daily or placebo group (1:1). The primary endpoint was the difference in the HbA1c level from baseline at week 24, and exploratory endpoints included the efficacy and safety of evogliptin over 52 weeks (trial registration: ClinicalTrials.gov NCT04170998). Results Evogliptin add-on to DAPA/MET therapy was superior in HbA1c reduction compared to placebo at weeks 24 and 52 (least square [LS] mean difference, –0.65% and –0.55%; 95% confidence interval [CI], –0.79 to –0.51 and –0.71 to –0.39; P<0.0001). The proportion of patients achieving HbA1c <7% was higher in the triple combination group at week 52 (32.14% vs. 8.51% in placebo; odds ratio, 5.62; P<0.0001). Evogliptin significantly reduced the fasting glucose levels and mean daily glucose levels with improvement in homeostatic model assessment of β-cell function (LS mean difference, 9.04; 95% CI, 1.86 to 16.21; P=0.0138). Adverse events were similar between the groups, and no serious adverse drug reactions were reported in the evogliptin group. Conclusion Long-term triple combination with evogliptin added to DAPA/MET showed superior HbA1c reduction and glycemic control compared to placebo at 52 weeks and was well tolerated

Genetic Drivers of Heterogeneity in Type 2 Diabetes Pathophysiology

Type 2 diabetes (T2D) is a heterogeneous disease that develops through diverse pathophysiological processes1,2 and molecular mechanisms that are often specific to cell type3,4. Here, to characterize the genetic contribution to these processes across ancestry groups, we aggregate genome-wide association study data from 2,535,601 individuals (39.7% not of European ancestry), including 428,452 cases of T2D. We identify 1,289 independent association signals at genome-wide significance (P \u3c 5 × 10-8) that map to 611 loci, of which 145 loci are, to our knowledge, previously unreported. We define eight non-overlapping clusters of T2D signals that are characterized by distinct profiles of cardiometabolic trait associations. These clusters are differentially enriched for cell-type-specific regions of open chromatin, including pancreatic islets, adipocytes, endothelial cells and enteroendocrine cells. We build cluster-specific partitioned polygenic scores5 in a further 279,552 individuals of diverse ancestry, including 30,288 cases of T2D, and test their association with T2D-related vascular outcomes. Cluster-specific partitioned polygenic scores are associated with coronary artery disease, peripheral artery disease and end-stage diabetic nephropathy across ancestry groups, highlighting the importance of obesity-related processes in the development of vascular outcomes. Our findings show the value of integrating multi-ancestry genome-wide association study data with single-cell epigenomics to disentangle the aetiological heterogeneity that drives the development and progression of T2D. This might offer a route to optimize global access to genetically informed diabetes care

Genetic drivers of heterogeneity in type 2 diabetes pathophysiology

Type 2 diabetes (T2D) is a heterogeneous disease that develops through diverse pathophysiological processes1,2 and molecular mechanisms that are often specific to cell type3,4. Here, to characterize the genetic contribution to these processes across ancestry groups, we aggregate genome-wide association study data from 2,535,601 individuals (39.7% not of European ancestry), including 428,452 cases of T2D. We identify 1,289 independent association signals at genome-wide significance (P &lt; 5 × 10-8) that map to 611 loci, of which 145 loci are, to our knowledge, previously unreported. We define eight non-overlapping clusters of T2D signals that are characterized by distinct profiles of cardiometabolic trait associations. These clusters are differentially enriched for cell-type-specific regions of open chromatin, including pancreatic islets, adipocytes, endothelial cells and enteroendocrine cells. We build cluster-specific partitioned polygenic scores5 in a further 279,552 individuals of diverse ancestry, including 30,288 cases of T2D, and test their association with T2D-related vascular outcomes. Cluster-specific partitioned polygenic scores are associated with coronary artery disease, peripheral artery disease and end-stage diabetic nephropathy across ancestry groups, highlighting the importance of obesity-related processes in the development of vascular outcomes. Our findings show the value of integrating multi-ancestry genome-wide association study data with single-cell epigenomics to disentangle the aetiological heterogeneity that drives the development and progression of T2D. This might offer a route to optimize global access to genetically informed diabetes care.</p