Duke Research Blog

Following the people and events that make up the research community at Duke.

Author: Lydia Goff (Page 1 of 2)

Coding: A Piece of Cake

Image result for cake

Imagine a cake, your favorite cake. Has your interest been piqued?

“Start with Cake” has proved an effective teaching strategy for Mine Cetinkaya-Rundel in her introduction-level statistics classes. In her talk “Teaching Computing via Visualization,” she lays out her classroom approaches to helping students maintain an interest in coding despite its difficulty. Just like a cooking class, a taste of the final product can motivate students to master the process. Cetinkaya-Rundel, therefore, believes that instead of having students begin with the flour and sugar and milk, they should dive right into the sweet frosting. While bringing cake to the first day of class has a great success rate for increasing a class’s attention span (they’ll sugar crash in their next classes, no worries), what this statistics professor actually refers to is showing the final visualizations. By giving students large amounts of pre-written code and only one or two steps to complete during the first few class periods, they can immediately recognize coding’s potential. The possibilities become exciting and capture their attention so that fewer students attempt to vanish with the magic of drop/add period. For the student unsure about coding, immediately writing their own code can seem overwhelming and steal the joy of creating.

Example of a visualization Cetinkaya-Rundel uses in her classes

To accommodate students with less background in coding, Cetinkaya-Rundel believes that skipping the baby steps proves a better approach than slowing the pace. By jumping straight into larger projects, students can spend more time wrestling their code and discovering the best strategies rather than memorizing the definition of a histogram. The idea is to give the students everything on day one, and then slowly remove the pre-written coding until they are writing on their own. The traditional classroom approach involves teaching students line-by-line until they have enough to create the desired visualizations. While Cetinkaya-Rundel admits that her style may not suit every individual and creating the assignments does require more time, she stands by her eat-dessert-first perspective on teaching. Another way she helps students maintain their original curiosity is by cherishing day one through pre-installed packages which allow students to start playing with visualizations and altering code right away.

Not only does Cetinkaya-Rundel give mouth-watering cakes as the end results for her students but she also sometimes shows them burnt and crumbling desserts. “People like to critique,” she explains as she lays out how to motivate students to begin writing original code. When she gives her students a sloppy graph and tells them to fix it, they are more likely to find creative solutions and explore how to make the graph most appealing to them. As the scaffolding falls away and students begin diverging from the style guides, Cetinkaya-Rundel has found that they have a greater understanding of and passion for coding. A spoonful of sugar really does help the medicine go down.  

    Post by Lydia Goff

Becoming the First: Nick Carnes

Editor’s Note: In the “Becoming the First” series,  first-generation college student and Rubenstein Scholar Lydia Goff explores the experiences of Duke researchers who were the first in their families to attend college.

A portrait of Duke Professor Nick Carnes

Nick Carnes

Should we care that we are governed by professionals and millionaires? This is one of the questions Nick Carnes, an assistant professor in the Sanford School of Public Policy, seeks to answer with his research. He explores unequal social class representation in the political process and how it affects policy making. But do any real differences even exist between politicians from lower socioeconomic classes and those from the upper classes? Carnes believes they do, not only because of his research but also because of his personal experiences.

When Carnes entered Princeton University as a political science graduate student, he was the only member of his cohort who had done restaurant, construction or factory work. While obtaining his undergraduate degree from the University of Tulsa, he worked twenty hours a week and during the summer clocked in at sixty to seventy hours a week between two jobs. He considered himself and his classmates “similar on paper,” just like how politicians from a variety of socioeconomic classes can also appear comparable. However, Carnes noticed that he approached some problems differently than his classmates and wondered why. After attributing his distinct approach to his working class background, without the benefits of established college graduate family members (his mother did go to college while he was growing up), he began developing his current research interests.

Carnes considers “challenging the negative stereotypes about working class people” the most important aspect of his research. When he entered college, his first meeting with his advisor was filled with confusion as he tried to decipher what a syllabus was. While his working class status did restrict his knowledge of college norms, he overcame these limitations. He is now a researcher, writer, and professor who considers his job “the best in the world” and whose own story proves that working class individuals can conquer positions more often inhabited by the experienced. As Carnes states, “There’s no good reason to not have working class people in office.” His research seeks to reinforce that.

His biggest challenge is that the data he needs to analyze does not exist in a well-documented manner. Much of his research involves gathering data so that he can generate results. His published book, White-Collar Government: The Hidden Role of Class in Economic Policy Making, and his book coming out in September, The Cash Ceiling: Why Only the Rich Run for Office–and What We Can Do About It, contain the data and results he has produced. Presently, he is beginning a project on transnational governments because “cash ceilings exist in every advanced democracy.” Carnes’ research proves we should care that professionals and millionaires run our government. Through his story, he exemplifies that students who come from families without generations of college graduates can still succeed.    

 

Post by Lydia Goff

 

Becoming the First: Erika Weinthal

Editor’s Note: In the “Becoming the First” series,  first-generation college student and Rubenstein Scholar Lydia Goff explores the experiences of Duke researchers who were the first in their families to attend college.

A portrait of Erika Weinthal

Erika Weinthal

In her corner office with a wall of windows and stuffed bookshelves, Erika Weinthal keeps a photo of her father. He came to the United States from Germany in 1940. And for a German Jew, that was extremely late. According to the family stories, Weinthal’s father left on the second to last boat from Italy. It is no surprise that he was never a big traveler after his arrival to America. As Weinthal describes it, “America…was the country that saved him.” Not only did it protect him, but it also gave his children opportunities that he did not have, such as going to college.

Weinthal, Lee Hill Snowdon Professor of Environmental Policy in Duke’s Nicholas School of the Environment, took this opportunity to become the first in her family to attend college, launching her career researching environmental policy and water security in areas including the former Soviet Union, Middle East, East Africa, India and the United States.

In high school, Weinthal traveled as an exchange student to Germany, a country her relatives could never understand her desire to visit. “As a child of a refugee, you didn’t talk about the war,” she explains as she describes how this silence created her curiosity about what happened. That journey to Bremen marked only the first of many trips around the world. In the Middle East, she examines environmental policy between countries that share water. In India, she has researched the relationship between wildlife and humans near protected areas. “What do you do when protected wildlife destroys crops and threatens livelihoods?” she asks, proving that since her curiosity about the war, she has not stopped asking questions.

However, her specific interest in environmental science and policy came straight from a different war: the Cold War. She became obsessed with everything Russian partly thanks to a high school teacher who agreed to teach her Russian one-on-one. The teacher introduced Weinthal to Russian literature and poetry. While her parents, like many parents, would have loved for her to become a doctor or a lawyer, they still trusted her when she enrolled in Oberlin College intent on studying Soviet politics. A class on Soviet environment politics further increased her interest in water security.

Currently, her work contends that water should be viewed as a basic human need separate from the political conflicts in Palestine and Israel. She has studied how protracted conflict in the region has led to the deterioration of water quality in the Gaza Strip, creating a situation in which water is now unfit for human consumption. Weinthal argues that these regions should not view water as property to be secured but rather as a human right they should guarantee.

Erika Weinthal’s father in 1940

As a child of a refugee and a first-generation college student, Weinthal says “you grow up essentially so grateful for what others have sacrificed for you.” Her dad believed in giving back to the next generation. He accomplished that goal and, in the process, gave the world a researcher who’s invested in environmental policy and human rights.

Post by Lydia Goff

 

DNA Breakage: What Doesn’t Kill You…

What doesn’t kill you makes you stronger―at least according to Kelly Clarkson’s recovery song for middle school crushes, philosopher Friedrich Nietzsche, and New York University researcher Viji Subramanian.

During the creation of sperm or eggs, DNA molecules exchange genetic material. This increases the differences between offspring and their parents and the overall species diversity and is thought to make an individual and a species stronger.

However, to trade genetic information — through a process called recombination — the DNA molecules must break at points along the chromosomes, risking permanent damage and loss of genomic integrity. In humans, errors during recombination can lead to infertility, fetal loss, and birth defects.

Subramanian, a postdoctoral researcher in the lab of Andreas Hochwagen at NYU, spoke at Duke on February 26. She studies how cells prevent excessive DNA breakage and how they regulate repair.

Subramanian uses budding yeast to study the ‘synaptonemal complex,’ a structure that forms between pairing chromosomes as shown in the above image. Over three hundred DNA breakage hotspots exist in the budding yeast’s synaptonemal complex. Normally, double-stranded DNA breaks go from none to some and then return to none.

However, when Subramanian removed the synaptonemal complex, the breaks still appeared, but they did not completely disappear by the end of the process. She  concluded that synaptonemal complex shuts down DNA break formation. The synaptonemal complex therefore is one way cells prevent excessive DNA breakage.

The formation of the synaptonemal complex

 

During DNA breakage repair, preference must occur between the pairing chromosomes in order for recombination to correctly transpire. A protein called Mek1 promotes this bias by suppressing DNA in select areas. Early in the process of DNA breakage and repair Mek1 levels are high, while synaptonemal complex density is low. Later, the synaptonemal complex increases while the Mek1 decreases.

This led to Subramanian’s conclusion that synaptonemal complex is responsible for removing Mek1, allowing in DNA repair. She then explored if the protein pch2 regulates the removal of Mek1. In pch2-mutant budding yeast cells, DNA breaks were not repaired.

Subramanian showed that at least one aspect of DNA breakage and repair occurs through the Mek1 protein suppression of repair, creating selectivity between chromosomes. The synaptonemal complex then uses pch2 to remove Mek1 allowing DNA breakage repair.

Subramanian had another question about this process though: how is breakage ensured in small chromosomes? Because there are fewer possible breaking points, the chance of recombination seems lower in small chromosomes. However, Subramanian discovered that zones of high DNA break potential exist near the chromosome ends, allowing numerous breaks to form even in smaller chromosomes. This explains why smaller chromosomes actually exhibit a higher density of DNA breaks and recombination since their end zones occupy a larger percentage of their total surface area.

In the future, Subramanian wants to continue studying the specific mechanics behind DNA breaks and repair, including how the chromosomes reorganize during and after this process. She is also curious about how Mek1 suppresses repair and has more than 200 Mek1 mutants in her current study.

Kelly Clarkson may prove that heartbreaks don’t destroy you, but Viji Subramanian proves that DNA breaks create a stronger, more unique genetic code.         

Post by Lydia Goff

        

Obesity: Do Your Cells Have a Sweet Tooth?

Obesity is a global public health crisis that has doubled since 1980. That is why Damaris N. Lorenzo, a professor of  Cell Biology and Physiology at UNC-Chapel Hill, has devoted her research to this topic.

Specifically, she examines the role of ankyrin-B variants in metabolism. Ankyrins play a role in the movement of substances such as ions into and out of the cell. One of the ways that ankyrins affect this movement is through the glucose transporter protein GLUT4 which is present in the heart, skeletal muscles, and insulin-responsive tissues. GLUT4 plays a large role in glucose levels throughout the entire body.

Through her research, Lorenzo discovered that with modern life spans and high calorie diets, ankyrin-B variants can be a risk factor for metabolic disease. She presented her work for the Duke Developmental & Stem Cell Biology department on March 7th.

Prevalence of Self-Reported Obesity Among U.S. Adults by State, 2016

GLUT4 helps remove glucose from the body’s circulation by moving it into cells. The more GLUT4, the more sugar cells absorb.

Ankyrin-B’s role in regulating GLUT4 therefore proves really important for overall health. Through experiments on mice, Lorenzo discovered that mice manipulated to have ankyrin-B mutations also had high levels of cell surface GLUT4. This led to increased uptake of glucose into cells. Ankyrin-B therefore regulates how quickly glucose enters adipocytes, cells that store fat. These ankyrin-B deficient mice end up with adipocytes that have larger lipid droplets, which are fatty acids.

Lorenzo was able to conclude that ankyrin-B deficiency leads to age-dependent obesity in mutant mice. Age-dependent because young ankyrin-B mutant mice with high fat diets are actually more likely to be affected by this change.

Obese mouse versus a regular mouse

Ankyrin-B has only recently been recognized as part of GLUT4 movement into the cell. As cell sizes grow through increased glucose uptake, not only does the risk of obesity rise but also inflammation is triggered and metabolism becomes impaired, leading to overall poor health.

With obesity becoming a greater problem due to increased calorie consumption, poor dietary habits, physical inactivity, environmental and life stressors, medical conditions, and drug treatments, understanding factors inside of the body can help. Lorenzo seeks to discover how ankyrin-B protein might play a role in the amount of sugar our cells internalize.

Post by Lydia Goff

How a Museum Became a Lab

Encountering and creating art may be some of mankind’s most complex experiences. Art, not just visual but also dancing and singing, requires the brain to understand an object or performance presented to it and then to associate it with memories, facts, and emotions.

A piece in Dario Robleto’s exhibit titled “The Heart’s Knowledge Will Decay” (2014)

In an ongoing experiment, Jose “Pepe” Contreras-Vidal and his team set up in artist Dario Robleto’s exhibit “The Boundary of Life Is Quietly Crossed” at the Menil Collection near downtown Houston. They then asked visitors if they were willing to have their trips through the museum and their brain activities recorded. Robleto’s work was displayed from August 16, 2014 to January 4, 2015. By engaging museum visitors, Contreras-Vidal and Robleto gathered brain activity data while also educating the public, combining research and outreach.

“We need to collect data in a more natural way, beyond the lab” explained Contreras-Vidal, an engineering professor at the University of Houston, during a talk with Robleto sponsored by the Nasher Museum.

More than 3,000 people have participated in this experiment, and the number is growing.

To measure brain activity, the volunteers wear EEG caps which record the electrical impulses that the brain uses for communication. EEG caps are noninvasive because they are just pulled onto the head like swim caps. The caps allow the museum goers to move around freely so Contreras-Vidal can record their natural movements and interactions.

By watching individuals interact with art, Contreras-Vidal and his team can find patterns between their experiences and their brain activity. They also asked the volunteers to reflect on their visit, adding a first person perspective to the experiment. These three sources of data showed them what a young girl’s favorite painting was, how she moved and expressed her reaction to this painting, and how her brain activity reflected this opinion and reaction.

The volunteers can also watch the recordings of their brain signals, giving them an opportunity to ask questions and engage with the science community. For most participants, this is the first time they’ve seen recordings of their brain’s electrical signals. In one trip, these individuals learned about art, science, and how the two can interact. Throughout this entire process, every member of the audience forms a unique opinion and learns something about both the world and themselves as they interact with and make art.

Children with EEG caps explore art.

Contreras-Vidal is especially interested in the gestures people make when exposed to the various stimuli in a museum and hopes to apply this information to robotics. In the future, he wants someone with a robotic arm to not only be able to grab a cup but also to be able to caress it, grip it, or snatch it. For example, you probably can tell if your mom or your best friend is approaching you by their footsteps. Contreras-Vidal wants to restore this level of individuality to people who have prosthetics.

Contreras-Vidal thinks science can benefit art just as much as art can benefit science. Both he and Robleto hope that their research can reduce many artists’ distrust of science and help advance both fields through collaboration.

Post by Lydia Goff

MyD88: Villain of Allergies and Asthma

Even if you don’t have allergies yourself, I guarantee you can list at least three people you know who have allergies. Asthma, a respiratory disorder commonly associated with allergies, afflicts over 300 million individuals worldwide.

Seddon Y. Thomas, PhD of the NIEHS

Seddon Y. Thomas, PhD of the NIEHS

Seddon Y. Thomas who works at the National Institute of Environmental Health Sciences has been exploring how sensitization to allergens occurs. The work, which she described at a recent  session of the Immunology Seminar Series, specifically focuses on the relationship between sensitization and the adaptor molecule MyD88.

MyD88 transfers signals between some of the proteins and receptors that are involved in immune responses to foreign invaders. Since allergies entail inflammation caused by an immune response, Thomas recognized that MyD88 played a role in the immune system’s sensitization to inhaled allergens.

Her research aims to discover how MyD88 alters conventional dendritic cells (cDCs) which are innate immune cells that drive allergic inflammation. MyD88 signaling in cDCs sometimes preserves open chromatin — the availability of DNA for rapid replication — which allows gene changes to happen quickly and in turn causes allergic sensitization. Open chromatin regions permit the DNA manipulation that can lead to allergies and asthma. 

Florescence microscopy image of mouse dendritic cells with mRNA-loaded blood cells.

To conduct her experiments, Thomas examines what happens in mice when she deletes MyD88 from lung epithelial cells and from antigen-presenting cells. Lung epithelial cells form a protective tissue where inhaled air meets the lung and protects from foreign invaders. But sometimes it takes its job a little too seriously and reacts strongly to allergens.

Similarly, antigen-presenting cells are involved in the immune system’s mission to protect the body, but can become confused about who the enemy is. When the signaling adaptor MyD88 is removed from lung epithelial cells, the number of eosinophils, inflammatory white blood cells, decreases. When it is removed from antigen-presenting cells, another type of white blood cell, neutrophils, also decreases.

Thomas said this shows that MyD88 is necessary for the inflammation in the lungs that causes asthma and allergies.

In her future research, Thomas wishes to explore dendritic cell gene expression, the molecular pathways controlling gene expression, and how specific types of lung epithelial cells adjust immune responses. Because MyD88 plays a role in the genetic changes, it makes sense to continue research on the genetic side.    

Post by Lydia Goff            

Morphogenesis: All Guts and Morning Glories

What is morphogenesis? Morphogenesis examines the development of the living organisms’ forms.

It also is an area of research for Lakshminarayanan Mahadevan, Professor of Applied Mathematics, Organismic and Evolutionary Biology and Physics at Harvard University. On his presentation in the Public Lectures Unveiling Math (PLUM) series here at Duke, he credited the beginnings of morphogenesis to D’Arcy Wentworth Thompson, author of the book On Growth and Form.

Mathematically, morphogenesis focuses on how different rates of growth change the shapes of organisms as they develop. Cell number, cell size, cell shape, and cell position comprise the primary cellular factors of multicellular morphogenesis, which studies larger structures than individual cells and is Mahadevan’s focus.

Effects on tissues appear through changes in sizes, connectivities, and shapes, altering the phenotype, or the outward physical appearance. All these variables change in space and time. Professor Mahadevan presented on morphogenesis studies that have been conducted on plant shoots, guts, and brains.

Research on plant shoots often concentrates on the question, “Why do plant shoots grow in such a wide variety of directions and what determines their shapes?” The picture below shows the different postures appearances of plant shoots from completely straight to leaning to hanging.

Can morphogenesis make sense of these differences? Through mathematical modeling, two stimuli for shoots’ shapes was determined: gravity and itself. Additionally, elasticity as a function of the shoots’ weight plays a role in the mathematical models of plant shoots’ shapes which appear in Mahadevan’s paper co-written with a fellow professor, Raghunath Chelakkot. Mahadevan also explored the formation of flower and leaf shapes with these morphogenesis studies. 

Over twenty feet of guts are coiled up inside you. In order to fit these intestines inside the mammals, they must coil and loop. But what variables determine how these guts loop around? To discover the answer to this question, Mahadevan and other researchers examined chick embryos which increase their gut lengths by a factor greater than twenty over a twelve-day span. They were able to create a physical model using a rubber tube sewn to a sheet that followed the same patterns as the chicks’ guts. Through their observation of not only chicks but also quail and mice, Mahadevan determined that the morphogenesis of the guts has no dependence on genetics or any other microscopic factors.

Mahadevan’s study of how the brain folds occurs through MRI images of human fetal development. Initially, barely any folding exists on fetal brains but eventually the geometry of the surrounding along with local stress forms folds on the brain. By creating a template with gel and treating it to mimic the relationship between the brain’s gray matter and white matter, Mahadevan along with other researchers discovered that they could reproduce the brain’s folds. Because they were able to recreate the folds through only global geometry and local stress, they concluded that morphogenesis evolution does not depend on microscopic factors such as genetics. Further, by examining if folding regions correlate with the activity regions of the brain, questions about the effect of physical form on abilities and the inner functions of the brain.

  

     

Scavenger Receptors in Environmental Lung Disease

“Lung disease causes 15% of deaths worldwide” Kymberly Gowdy explained in her lecture at Duke,  “Clean Up and Clear Out: A Novel Role for Scavenger Receptors in Environmental Lung Disease.”

In her research, she applies her training as an immunologist to analyze immune responses to environmental challenges and their role in lung disease. Gowdy is an Assistant Professor at East Carolina University where her research specifically focuses on scavenger receptors (SRs). SRs are pattern recognition receptors that recognize and bind cellular debris and pathogens. Gowdy’s research focuses on scavenger receptor SR-B1 and SR-CD163.

Kymberly Gowdy of East Carolina University

Kymberly Gowdy of East Carolina University

Her experiments with SR-B1 have shown that knockout mice (mice without the scavenger receptor B1) have increased mortality rates after pulmonary infection, as shown in the figure below. After examining different causes of this increase in mortality, Gowdy and her lab concluded that the cause was an increase in bacterial burden.

The pattern they detected revealed that an increase of bacteria in the blood correlates to both an increase in cytokines (substances secreted by immune cells that create inflammation and respond to infections) and an increase in mortality. Gowdy also associated a decrease in clearance in the lungs with this trend, which explains why pneumonia does not heal and therefore leads to death.

Gowdy’s lab also explored the possibility for a connection between SR-B1 and ozone-induced respiratory and cardiovascular inflammation. She discovered a positive correlation between SR-B1, the oxidization of lipids in the lungs, and pulmonary inflammation. She concludes that SR-B1 expression is protective against air pollutant exposure such as ozone.

Mice lacking SR-B1 (dashed line) only survived two days after an infection challenged their lungs.

Gowdy has also investigated a receptor called SR-CD163 which clears hemoglobin and haptoglobin (Hb-Hp) from the lungs. This receptor protects organs from cell-free hemoglobin preventing damage. When she exposed knockout mice without SR-CD163 to ozone, she discovered an increase in the pulmonary levels of cell-free hemoglobin. Similarly to experiments with SR-B1, the CD163-deficient mice demonstrated patterns of increased lung damage as they experienced increased exposure to ozone.

Through her collaboration with laboratories at Duke, Gowdy has been able to discover that ozone exposure increases the response of pulmonary CD163 in mice and humans.

Gowdy’s work has shown the existence of direct relationships between environmental factors such as ozone and the levels of scavenger receptors such as B1 and CD163 in the lungs. The complex association between immune responses and lung diseases creates an interesting field of research, particularly when explored through the lens of environmental triggers.

Gowdy’s results reveal the intricacy of the immune system. An inflammatory response is meant to protect an individual’s health, but too much immune activation in the lungs can lead to disease.

Post by Lydia Goff.

Who Gets Sick and Why?

During his presentation as part of the Chautauqua lecture series, Duke sociologist Dr. Tyson Brown explained his research exploring the ways racial inequalities affect a person’s health later in life. His project mainly looks at the Baby Boomer generation, Americans born between 1946 and 1964.

With incredible increases in life expectancy, from 47 years in 1900 to 79 today, elderly people are beginning to form a larger percentage of the population. However among black people, the average life expectancy is three and a half years shorter.

“Many of you probably do not think that three and half years is a lot,” Brown said. “But imagine how much less time that is with your family and loved ones. In the end, I think all of us agree we want those extra three and a half years.”

Not only does the black population in America have shorter lives on average but they also tend to have sicker lives with higher blood pressures, greater chances of stroke, and higher probability of diabetes. In total, the number of deaths that would be prevented if African-American people had the same life expectancy as white people is 880,000 over a nine-year span. Now, the question Brown has challenged himself with is “Why does this discrepancy occur?”

Brown said he first concluded that health habits and behaviors do not create this life expectancy gap because white and black people have similar rates of smoking, drinking, and illegal drug use. He then decided to explore socioeconomic status. He discovered that as education increases, mortality decreases. And as income increases, self-rated health increases. He said that for every dollar a white person makes, a black person makes 59 cents.

This inequality in income points to the possible cause for the racial inequality in health, he said.  Additionally, in terms of wealth instead of income, a black person has 6 cents compared to the white person’s dollar. Possibly even more concerning than this inconsistency is the fact that it has gotten worse, not better, over time. Before the 2006 recession, blacks had 10-12 cents of wealth for every white person’s dollar.

Brown believes that this financial stress forms one of many stressors in black lives including chronic stressors, everyday discrimination, traumatic events, and neighborhood disorder which affect their health.

Over time, these stressors create something called physiological dysregulation, otherwise known as wear and tear, through repeated activation of  the stress response, he said. Recognition of the prevalence of these stressors in black lives has lead to Brown’s next focus on the extent of the effect of stressors on health. For his data, he uses the Health and Retirement Study and self-rated health (proven to predict mortality better than physician evaluations). For his methods, he employs structural equation modeling. Racial inequalities in socioeconomic resources, stressors and biomarkers of physiological dysregulation collectively explain 87% of the health gap with any number of causes capable of filling the remaining percentage.

Brown said his next steps include using longitudinal and macro-level data on structural inequality to understand how social inequalities “get under the skin” over a person’s lifetime. He suggests that the next steps for society, organizations, and the government to decrease this racial discrepancy rest in changing economic policy, increasing wages, guaranteeing work, and reducing residential segregation.

Post by Lydia Goff

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