Cohort bias in predictive risk assessments of future criminal justice system involvement.

Risk assessment instruments (RAIs) are widely used to aid high-stakes decision-making in criminal justice settings and other areas such as health care and child welfare. These tools, whether using machine learning or simpler algorithms, typically assume a time-invariant relationship between predictors and outcome. Because societies are themselves changing and not just individuals, this assumption may be violated in many behavioral settings, generating what we call cohort bias. Analyzing criminal histories in a cohort-sequential longitudinal study of children, we demonstrate that regardless of model type or predictor sets, a tool trained to predict the likelihood of arrest between the ages of 17 and 24 y on older birth cohorts systematically overpredicts the likelihood of arrest for younger birth cohorts over the period 1995 to 2020. Cohort bias is found for both relative and absolute risks, and it persists for all racial groups and within groups at highest risk for arrest. The results imply that cohort bias is an underappreciated mechanism generating inequality in contacts with the criminal legal system that is distinct from racial bias. Cohort bias is a challenge not only for predictive instruments with respect to crime and justice, but also for RAIs more broadly.

Adult Children of the Prison Boom: Family Troubles and the Intergenerational Transmission of Criminal Justice Contact.

Intergenerational transmission processes have long been of interest to demographers, but prior research on the intergenerational transmission of criminal justice contact is relatively sparse and limited by its lack of attention to the correlated "family troubles" and familial incarceration that predate criminal justice contact. In this article, we provide a test of the intergenerational transmission of criminal justice contact after adjusting extensively for these factors that predate such contact by linking longitudinal data from the Project on Human Development in Chicago Neighborhoods with official arrest histories from 1995 to 2020. The results provide support for three conclusions. First, parental criminal justice contact is associated with a shorter time to first arrest and a larger number of arrests even after rigorously accounting for selection. Second, robustness checks demonstrate that neither the magnitude nor the significance of the findings is sensitive to model choices. Third, associations are strongest among White individuals and inconsistently significant for African American and Hispanic individuals. Despite large recent crime declines, the results indicate that parental criminal justice contact elevates the criminal justice contact of the adult children of the prison boom, independent of the often-overlooked troubles that predate criminal justice contact, and that these associations are strongest among the White population.

Social change and cohort differences in group-based arrest trajectories over the last quarter-century.

This article draws on official criminal histories for multiple birth cohorts spanning a 17-y difference in birth year to study how social change can alter our understanding of influential theories and policies about criminal offender groups. Arrest histories are linked to comprehensive longitudinal measurement on over 1,000 individuals originally from Chicago. Using group-based trajectory modeling, we investigated the magnitude and type of cohort differences in trajectories of arrest over the period 1995 to 2020. Our results show that trajectory group membership varies strongly by birth cohort. Membership in the nonoffender group is nearly 15 percentage points higher for cohorts born in the mid-1990s as compared to those born in the 1980s; conversely, older cohorts are more likely to be members of adolescent-limited and chronic-offender groups. Large cohort differences in trajectory group membership persist after controlling for a wide-ranging set of demographic characteristics and early-life risk factors that vary by cohort and that prior research has identified as important influences on crime. Not only does the effect of social change on cohort differentiation persist, but its magnitude is comparable to-indeed larger than-differences in trajectory group membership associated with varying levels of self-control or by whether individuals grew up in high-poverty households. These results suggest that changes in the broader social environment shared by members of the same birth cohort are as powerful in shaping their trajectory group membership as classic predictors identified in prior research, a finding that carries implications for crime-control policies that rely on prediction.

Punishing and toxic neighborhood environments independently predict the intergenerational social mobility of black and white children.

We use data on intergenerational social mobility by neighborhood to examine how social and physical environments beyond concentrated poverty predict children's long-term well-being. First, we examine neighborhoods that are harsh on children's development: those characterized by high levels of violence, incarceration, and lead exposure. Second, we examine potential supportive or offsetting mechanisms that promote children's development, such as informal social control, cohesion among neighbors, and organizational participation. Census tract mobility estimates from linked income tax and Census records are merged with surveys and administrative records in Chicago. We find that exposure to neighborhood violence, incarceration, and lead combine to independently predict poor black boys' later incarceration as adults and lower income rank relative to their parents, and poor black girls' teenage motherhood. Features of neighborhood social organization matter less, but are selectively important. Results for poor whites also show that toxic environments independently predict lower social mobility, as do features of social organization, to a lesser extent. Overall, our measures contribute a 76% relative increase in explained variance for black male incarceration beyond that of concentrated poverty and other standard characteristics, an 18% increase for black male income rank (70% for whites), and a 17% increase for teenage motherhood of black girls (40% for whites).

Late neuroprogenitors contribute to normal retinal vascular development in a Hif2a-dependent manner.

In the adult central nervous system, endothelial and neuronal cells engage in tight cross-talk as key components of the so-called neurovascular unit. Impairment of this important relationship adversely affects tissue homeostasis, as observed in neurodegenerative conditions including Alzheimer's and Parkinson's disease. In development, the influence of neuroprogenitor cells on angiogenesis is poorly understood. Here, we show in mouse that these cells interact intimately with the growing retinal vascular network, and we identify a novel regulatory mechanism of vasculature development mediated by hypoxia-inducible factor 2a (Hif2a). By Cre-lox gene excision, we show that Hif2a in retinal neuroprogenitor cells upregulates the expression of the pro-angiogenic mediators vascular endothelial growth factor and erythropoietin, whereas it locally downregulates the angiogenesis inhibitor endostatin. Importantly, absence of Hif2a in retinal neuroprogenitor cells causes a marked reduction of proliferating endothelial cells at the angiogenic front. This results in delayed retinal vascular development, fewer major retinal vessels and reduced density of the peripheral deep retinal vascular plexus. Our findings demonstrate that retinal neuroprogenitor cells are a crucial component of the developing neurovascular unit.

Urban mobility and neighborhood isolation in America's 50 largest cities.

Influential research on the negative effects of living in a disadvantaged neighborhood assumes that its residents are socially isolated from nonpoor or "mainstream" neighborhoods, but the extent and nature of such isolation remain in question. We develop a test of neighborhood isolation that improves on static measures derived from commonly used census reports by leveraging fine-grained dynamic data on the everyday movement of residents in America's 50 largest cities. We analyze 650 million geocoded Twitter messages to estimate the home locations and travel patterns of almost 400,000 residents over 18 mo. We find surprisingly high consistency across neighborhoods of different race and income characteristics in the average travel distance (radius) and number of neighborhoods traveled to (spread) in the metropolitan region; however, we uncover notable differences in the composition of the neighborhoods visited. Residents of primarily black and Hispanic neighborhoods-whether poor or not-are far less exposed to either nonpoor or white middle-class neighborhoods than residents of primarily white neighborhoods. These large racial differences are notable given recent declines in segregation and the increasing diversity of American cities. We also find that white poor neighborhoods are substantially isolated from nonpoor white neighborhoods. The results suggest that even though residents of disadvantaged neighborhoods travel far and wide, their relative isolation and segregation persist.

Stabilization of myeloid-derived HIFs promotes vascular regeneration in retinal ischemia.

The retinal vasculature is tightly organized in a structure that provides for the high metabolic demand of neurons while minimizing interference with incident light. The adverse impact of retinal vascular insufficiency is mitigated by adaptive vascular regeneration but exacerbated by pathological neovascularization. Aberrant growth of neovessels in the retina is responsible for impairment of sight in common blinding disorders including retinopathy of prematurity, proliferative diabetic retinopathy, and age-related macular degeneration. Myeloid cells are key players in this process, with diverse roles that can either promote or protect against ocular neovascularization. We have previously demonstrated that myeloid-derived VEGF, HIF1, and HIF2 are not essential for pathological retinal neovascularization. Here, however, we show by cell-specific depletion of Vhl in a mouse model of retinal ischemia (oxygen-induced retinopathy, OIR) that myeloid-derived HIFs promote VEGF and bFGF expression and enhance vascular regeneration in association with improved density and organization of the astrocytic network.

Skill-Based Contextual Sorting: How Parental Cognition and Residential Mobility Produce Unequal Environments for Children.

Highly skilled parents deploy distinct strategies to cultivate their children's development, but little is known about how parental cognitive skills interact with metropolitan opportunity structures and residential mobility to shape a major domain of inequality in children's lives: the neighborhood. We integrate multiple literatures to develop hypotheses on parental skill-based sorting by neighborhood socioeconomic status and public school test scores, which we test using an original follow-up of the Los Angeles Family and Neighborhood Survey. These data include more than a decade's worth of residential histories for households with children that are linked to census, geographic information system, and educational administrative data. We construct discrete-choice models of neighborhood selection that account for heterogeneity among household types, incorporate the unique spatial structure of Los Angeles County, and include a wide range of neighborhood factors. The results show that parents' cognitive skills interact with neighborhood socioeconomic status to predict residential selection after accounting for, and confirming, the expected influences of race, income, education, housing market conditions, and spatial proximity. Among parents in the upper/upper-middle class, cognitive skills predict sorting on average public school test scores rather than neighborhood socioeconomic status. Overall, we reveal skill-based contextual sorting as an overlooked driver of urban stratification.

Urban sustainability in an age of enduring inequalities: Advancing theory and ecometrics for the 21st-century city.

The environmental fragility of cities under advanced urbanization has motivated extensive efforts to promote the sustainability of urban ecosystems and physical infrastructures. Less attention has been devoted to neighborhood inequalities and fissures in the civic infrastructure that potentially challenge social sustainability and the capacity of cities to collectively address environmental challenges. This article draws on a program of research in three American cities-Boston, Chicago, and Los Angeles-to develop hypotheses and methodological strategies for assessing how the multidimensional and multilevel inequalities that characterize contemporary cities bear on sustainability. In addition to standard concerns with relative inequality in income, the article reviews evidence on compounded deprivation, racial cleavages, civic engagement, institutional cynicism, and segregated patterns of urban mobility and organizational ties that differentially connect neighborhood resources. Harnessing "ecometric" measurement tools and emerging sources of urban data with a theoretically guided framework on neighborhood inequality can enhance the pursuit of sustainable cities, both in the United States and globally.

Prevention of Photoreceptor Cell Loss in a Cln6nclf Mouse Model of Batten Disease Requires CLN6 Gene Transfer to Bipolar Cells.

The neuronal ceroid lipofuscinoses (NCLs) are inherited lysosomal storage disorders characterized by general neurodegeneration and premature death. Sight loss is also a major symptom in NCLs, severely affecting the quality of life of patients, but it is not targeted effectively by brain-directed therapies. Here we set out to explore the therapeutic potential of an ocular gene therapy to treat sight loss in NCL due to a deficiency in the transmembrane protein CLN6. We found that, although Cln6nclf mice presented mainly with photoreceptor degeneration, supplementation of CLN6 in photoreceptors was not beneficial. Because the level of CLN6 is low in photoreceptors but high in bipolar cells (retinal interneurons that are only lost in Cln6-deficient mice at late disease stages), we explored the therapeutic effects of delivering CLN6 to bipolar cells using adeno-associated virus (AAV) serotype 7m8. Bipolar cell-specific expression of CLN6 slowed significantly the loss of photoreceptor function and photoreceptor cells. This study shows that the deficiency of a gene normally expressed in bipolar cells can cause the loss of photoreceptors and that this can be prevented by bipolar cell-directed treatment.

Activation of podocyte Notch mediates early Wt1 glomerulopathy.

The Wilms' tumor suppressor gene, WT1, encodes a zinc finger protein that regulates podocyte development and is highly expressed in mature podocytes. Mutations in the WT1 gene are associated with the development of renal failure due to the formation of scar tissue within glomeruli, the mechanisms of which are poorly understood. Here, we used a tamoxifen-based CRE-LoxP system to induce deletion of Wt1 in adult mice to investigate the mechanisms underlying evolution of glomerulosclerosis. Podocyte apoptosis was evident as early as the fourth day post-induction and increased during disease progression, supporting a role for Wt1 in mature podocyte survival. Podocyte Notch activation was evident at disease onset with upregulation of Notch1 and its transcriptional targets, including Nrarp. There was repression of podocyte FoxC2 and upregulation of Hey2 supporting a role for a Wt1/FoxC2/Notch transcriptional network in mature podocyte injury. The expression of cleaved Notch1 and HES1 proteins in podocytes of mutant mice was confirmed in early disease. Furthermore, induction of podocyte HES1 expression was associated with upregulation of genes implicated in epithelial mesenchymal transition, thereby suggesting that HES1 mediates podocyte EMT. Lastly, early pharmacological inhibition of Notch signaling ameliorated glomerular scarring and albuminuria. Thus, loss of Wt1 in mature podocytes modulates podocyte Notch activation, which could mediate early events in WT1-related glomerulosclerosis.

From Lead Exposure in Early Childhood to Adolescent Health: A Chicago Birth Cohort.

OBJECTIVES: To assess the relationships between childhood lead exposure and 3 domains of later adolescent health: mental, physical, and behavioral. METHODS: We followed a random sample of birth cohort members from the Project on Human Development in Chicago Neighborhoods, recruited in 1995 to 1997, to age 17 years and matched to childhood blood test results from the Department of Public Health. We used ordinary least squares regression, coarsened exact matching, and instrumental variables to assess the relationship between average blood lead levels in childhood and impulsivity, anxiety or depression, and body mass index in adolescence. All models adjusted for relevant individual, household, and neighborhood characteristics. RESULTS: After adjustment, a 1 microgram per deciliter increase in average childhood blood lead level significantly predicts 0.06 (95% confidence interval [CI] = 0.01, 0.12) and 0.09 (95% CI = 0.03, 0.16) SD increases and a 0.37 (95% CI = 0.11, 0.64) point increase in adolescent impulsivity, anxiety or depression, and body mass index, respectively, following ordinary least squares regression. Results following matching and instrumental variable strategies are very similar. CONCLUSIONS: Childhood lead exposure undermines adolescent well-being, with implications for the persistence of racial and class inequalities, considering structural patterns of initial exposure.

Flow cytometric analysis of inflammatory and resident myeloid populations in mouse ocular inflammatory models.

Myeloid cells make a pivotal contribution to tissue homeostasis during inflammation. Both tissue-specific resident populations and infiltrating myeloid cells can cause tissue injury through aberrant activation and/or dysregulated activity. Reliable identification and quantification of myeloid cells within diseased tissues is important to understand pathological inflammatory processes. Flow cytometry is a valuable technique for leukocyte analysis, but a standardized flow cytometric method for myeloid cell populations in the eye is lacking. Here, we validate a reproducible flow cytometry gating approach to characterize myeloid cells in several commonly used models of ocular inflammation. We profile and quantify myeloid subsets across these models, and highlight the value of this strategy in identifying phenotypic differences using Ccr2-deficient mice. This method will aid standardization in the field and facilitate future investigations into the roles of myeloid cells during ocular inflammation.

Monocyte/Macrophage-derived IGF-1 Orchestrates Murine Skeletal Muscle Regeneration and Modulates Autocrine Polarization.

Insulin-like growth factor 1 (IGF-1) is a potent enhancer of tissue regeneration, and its overexpression in muscle injury leads to hastened resolution of the inflammatory phase. Here, we show that monocytes/macrophages constitute an important initial source of IGF-1 in muscle injury, as conditional deletion of the IGF-1 gene specifically in mouse myeloid cells (ϕIGF-1 CKO) blocked the normal surge of local IGF-1 in damaged muscle and significantly compromised regeneration. In injured muscle, Ly6C+ monocytes/macrophages and CD206+ macrophages expressed equivalent IGF-1 levels, which were transiently upregulated during transition from the inflammation to repair. In injured ϕIGF-1 CKO mouse muscle, accumulation of CD206+ macrophages was impaired, while an increase in Ly6C+ monocytes/macrophages was favored. Transcriptional profiling uncovered inflammatory skewing in ϕIGF-1 CKO macrophages, which failed to fully induce a reparative gene program in vitro or in vivo, revealing a novel autocrine role for IGF-1 in modulating murine macrophage phenotypes. These data establish local macrophage-derived IGF-1 as a key factor in inflammation resolution and macrophage polarization during muscle regeneration.

Cardiac-Restricted IGF-1Ea Overexpression Reduces the Early Accumulation of Inflammatory Myeloid Cells and Mediates Expression of Extracellular Matrix Remodelling Genes after Myocardial Infarction.

Strategies to limit damage and improve repair after myocardial infarct remain a major therapeutic goal in cardiology. Our previous studies have shown that constitutive expression of a locally acting insulin-like growth factor-1 Ea (IGF-1Ea) propeptide promotes functional restoration after cardiac injury associated with decreased scar formation. In the current study, we investigated the underlying molecular and cellular mechanisms behind the enhanced functional recovery. We observed improved cardiac function in mice overexpressing cardiac-specific IGF-1Ea as early as day 7 after myocardial infarction. Analysis of gene transcription revealed that supplemental IGF-1Ea regulated expression of key metalloproteinases (MMP-2 and MMP-9), their inhibitors (TIMP-1 and TIMP-2), and collagen types (Col 1α1 and Col 1α3) in the first week after injury. Infiltration of inflammatory cells, which direct the remodelling process, was also altered; in particular there was a notable reduction in inflammatory Ly6C+ monocytes at day 3 and an increase in anti-inflammatory CD206+ macrophages at day 7. Taken together, these results indicate that the IGF-1Ea transgene shifts the balance of innate immune cell populations early after infarction, favouring a reduction in inflammatory myeloid cells. This correlates with reduced extracellular matrix remodelling and changes in collagen composition that may confer enhanced scar elasticity and improved cardiac function.

Achieving the Middle Ground in an Age of Concentrated Extremes: Mixed Middle-Income Neighborhoods and Emerging Adulthood.

This article focuses on stability and change in "mixed middle-income" neighborhoods. We first analyze variation across nearly two decades for all neighborhoods in the United States and in the Chicago area, particularly. We then analyze a new longitudinal study of almost 700 Chicago adolescents over an 18-year span, including the extent to which they are exposed to different neighborhood income dynamics during the transition to young adulthood. The concentration of income extremes is persistent among neighborhoods, generally, but mixed middle-income neighborhoods are more fluid. Persistence also dominates among individuals, though Latino-Americans are much more likely than African Americans or whites to be exposed to mixed middle-income neighborhoods in the first place and to transition into them over time, even when adjusting for immigrant status, education, income, and residential mobility. The results here enhance our knowledge of the dynamics of income inequality at the neighborhood level, and the endurance of concentrated extremes suggests that policies seeking to promote mixed-income neighborhoods face greater odds than commonly thought.

T-cell immunophenotyping distinguishes active from latent tuberculosis.

BACKGROUND: Changes in the phenotype and function of Mycobacterium tuberculosis (M. tuberculosis)-specific CD4+ and CD8+ T-cell subsets in response to stage of infection may allow discrimination between active tuberculosis and latent tuberculosis infection. METHODS: A prospective comparison of M. tuberculosis-specific cellular immunity in subjects with active tuberculosis and latent tuberculosis infection, with and without human immunodeficiency virus (HIV) coinfection. Polychromatic flow cytometry was used to measure CD4+ and CD8+ T-cell subset phenotype and secretion of interferon γ (IFN-γ), interleukin 2 (IL-2), and tumor necrosis factor α (TNF-α). RESULTS: Frequencies of CD4+ and CD8+ cells secreting IFN-γ-only, TNF-α-only and dual IFN-γ/TNF-α were greater in active tuberculosis vs latent tuberculosis infection. All M. tuberculosis-specific CD4+ subsets, with the exception of IL-2-only cells, switched from central to effector memory phenotype in active tuberculosis vs latent tuberculosis infection, accompanied by a reduction in IL-7 receptor α (CD127) expression. The frequency of PPDspecific CD4+ TNF-α-only-secreting T cells with an effector phenotype accurately distinguished active tuberculosis from latent tuberculosis infection with an area under the curve of 0.99, substantially more discriminatory than measurement of function alone. CONCLUSIONS: Combined measurement of T-cell phenotype and function defines a highly discriminatory biomarker of tuberculosis disease activity. Unlocking the diagnostic and monitoring potential of this combined approach now requires validation in large-scale prospective studies.

Juvenile Arrest and Collateral Educational Damage in the Transition to Adulthood.

Official sanctioning of students by the criminal justice system is a long-hypothesized source of educational disadvantage, but its explanatory status remains unresolved. Few studies of the educational consequences of a criminal record account for alternative explanations such as low self-control, lack of parental supervision, deviant peers, and neighborhood disadvantage. Moreover, virtually no research on the effect of a criminal record has examined the "black box" of mediating mechanisms or the consequence of arrest for postsecondary educational attainment. Analyzing longitudinal data with multiple and independent assessments of theoretically relevant domains, this paper estimates the direct effect of arrest on later high school dropout and college enrollment for adolescents with otherwise equivalent neighborhood, school, family, peer, and individual characteristics as well as similar frequency of criminal offending. We present evidence that arrest has a substantively large and robust impact on dropping out of high school among Chicago public school students. We also find a significant gap in four-year college enrollment between arrested and otherwise similar youth without a criminal record. We assess intervening mechanisms hypothesized to explain the process by which arrest disrupts the schooling process, and, in turn, produces collateral educational damage. The results imply that institutional responses and disruptions in students' educational trajectories, rather than social psychological factors, are responsible for the arrest-education link.