Slogging and Stumbling Toward Social Justice in a Private Elementary School: The Complicated Case of St. Malachy

This case study examines St. Malachy, an urban Catholic elementary school primarily serving children traditionally marginalized by race, class, linguistic heritage, and disability. As a private school, St. Malachy serves the public good by recruiting and retaining such traditionally marginalized students. As empirical studies involving Catholic schools frequently juxtapose them with public schools, the author presents this examination from a different tack. Neither vilifying nor glorifying Catholic schooling, this study critically examines the pursuit of social justice in this school context. Data gathered through a 1-year study show that formal and informal leaders in St. Malachy adapted their governance, aggressively sought community resources, and focused their professional development to build the capacity to serve their increasingly pluralistic student population. The analysis confirms the deepening realization that striving toward social justice is a messy, contradictory, and complicated pursuit, and that schools in both public and private sectors are allies in this pursuit

Synaptic processes and immune-related pathways implicated in Tourette syndrome.

Tourette syndrome (TS) is a neuropsychiatric disorder of complex genetic architecture involving multiple interacting genes. Here, we sought to elucidate the pathways that underlie the neurobiology of the disorder through genome-wide analysis. We analyzed genome-wide genotypic data of 3581 individuals with TS and 7682 ancestry-matched controls and investigated associations of TS with sets of genes that are expressed in particular cell types and operate in specific neuronal and glial functions. We employed a self-contained, set-based association method (SBA) as well as a competitive gene set method (MAGMA) using individual-level genotype data to perform a comprehensive investigation of the biological background of TS. Our SBA analysis identified three significant gene sets after Bonferroni correction, implicating ligand-gated ion channel signaling, lymphocytic, and cell adhesion and transsynaptic signaling processes. MAGMA analysis further supported the involvement of the cell adhesion and trans-synaptic signaling gene set. The lymphocytic gene set was driven by variants in FLT3, raising an intriguing hypothesis for the involvement of a neuroinflammatory element in TS pathogenesis. The indications of involvement of ligand-gated ion channel signaling reinforce the role of GABA in TS, while the association of cell adhesion and trans-synaptic signaling gene set provides additional support for the role of adhesion molecules in neuropsychiatric disorders. This study reinforces previous findings but also provides new insights into the neurobiology of TS

Centrality Dependence Of The Pseudorapidity Density Distribution For Charged Particles In Pb-pb Collisions At √snn=2.76tev

7264/Mai61062

Long-range Angular Correlations On The Near And Away Side In P-pb Collisions At √snn=5.02 Tev

7191/Mar294

A Mechanistic Framework for Understanding the Effects of Climate Change on the Link Between Flowering and Fruiting Phenology

Phenological shifts are a widely studied consequence of climate change. Little is known, however, about certain critical phenological events, nor about mechanistic links between shifts in different life-history stages of the same organism. Among angiosperms, flowering times have been observed to advance with climate change, but, whether fruiting times shift as a direct consequence of shifting flowering times, or respond differently or not at all to climate change, is poorly understood. Yet, shifts in fruiting could alter species interactions, including by disrupting seed dispersal mutualisms. In the absence of long-term data on fruiting phenology, but given extensive data on flowering, we argue that an understanding of whether flowering and fruiting are tightly linked or respond independently to environmental change can significantly advance our understanding of how fruiting phenologies will respond to warming climates. Through a case study of biotically and abiotically dispersed plants, we present evidence for a potential functional link between the timing of flowering and fruiting. We then propose general mechanisms for how flowering and fruiting life history stages could be functionally linked or independently driven by external factors, and we use our case study species and phenological responses to distinguish among proposed mechanisms in a real-world framework. Finally, we identify research directions that could elucidate which of these mechanisms drive the timing between subsequent life stages. Understanding how fruiting phenology is altered by climate change is essential for all plant species but is particularly critical to sustaining the large numbers of plant species that rely on animal-mediated dispersal, as well as the animals that rely on fruit for sustenance. Copyright © 2021 Sandor, Aslan, Pejchar and Bronstein.Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Lifetime prevalence, age of risk, and genetic relationships of comorbid psychiatric disorders in Tourette syndrome

Importance: Tourette syndrome (TS) is characterized by high rates of psychiatric comorbidity; however, fewstudies have fully characterized these comorbidities. Furthermore, most studies have included relatively fewparticipants (< 200), and none has examined the ages of highest risk for each TS-associated comorbidity or their etiologic relationship to TS.Objective: To characterize the lifetime prevalence, clinical associations, ages of highest risk, and etiology of psychiatric comorbidity among individuals with TS.Design, Setting, And Participants: Cross-sectional structured diagnostic interviews conducted between April 1, 1992, and December 31, 2008, of participants with TS (n = 1374) and TS-unaffected family members (n = 1142).Main Outcomes And Measures: Lifetime prevalence of comorbid DSM-IV-TR disorders, their heritabilities, ages of maximal risk, and associations with symptom severity, age at onset, and parental psychiatric history.Results: The lifetime prevalence of any psychiatric comorbidity among individuals with TS was 85.7%; 57.7%of the population had 2 or more psychiatric disorders. The mean (SD) number of lifetime comorbid diagnoses was 2.1 (1.6); the mean number was 0.9 (1.3) when obsessive-compulsive disorder (OCD) and attention-deficit/hyperactivity disorder (ADHD) were excluded, and 72.1% of the individuals met the criteria for OCD or ADHD. Other disorders, including mood, anxiety, and disruptive behavior, each occurred in approximately 30% of the participants. The age of greatest risk for the onset of most comorbid psychiatric disorders was between 4 and 10 years, with the exception of eating and substance use disorders, which began in adolescence (interquartile range, 15-19 years for both). Tourette syndrome was associated with increased risk of anxiety (odds ratio [OR], 1.4; 95%CI, 1.0-1.9; P = .04) and decreased risk of substance use disorders (OR, 0.6; 95%CI, 0.3-0.9; P = .02) independent from comorbid OCD and ADHD; however, high rates of mood disorders among participants with TS (29.8%)may be accounted for by comorbid OCD (OR, 3.7; 95%CI, 2.9-4.8; P < .001). Parental history of ADHD was associated with a higher burden of non-OCD, non-ADHD comorbid psychiatric disorders (OR, 1.86; 95%CI, 1.32-2.61; P < .001). Genetic correlations between TS and mood (RhoG, 0.47), anxiety (RhoG, 0.35), and disruptive behavior disorders (RhoG, 0.48), may be accounted for by ADHD and, for mood disorders, by OCD.Conclusions And Relevance: This study is, to our knowledge, the most comprehensive of its kind. It confirms the belief that psychiatric comorbidities are common among individuals with TS, demonstrates that most comorbidities begin early in life, and indicates that certain comorbiditiesmay be mediated by the presence of comorbid OCD or ADHD. In addition, genetic analyses suggest that some comorbiditiesmay be more biologically related to OCD and/or ADHD rather than to TS