38 research outputs found

    Midwest Evaluation of the Adult Functioning of Former Foster Youth

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    The Midwest Evaluation of the Adult Functioning of Former Foster Youth (Midwest Study) is a prospective study that has been following a sample of young people from Iowa, Wisconsin, and Illinois as they transition out of foster care into adulthood. It is a collaborative effort involving Chapin Hall at the University of Chicago; Partners for Our Children at the University of Washington, Seattle; the University of Wisconsin Survey Center; and the public child welfare agencies in Illinois, Iowa, and Wisconsin.The Midwest Study provides a comprehensive picture of how foster youth are faring during this transition since the Foster Care Independence Act of 1999 became law. Foster youth in Iowa, Wisconsin, and Illinois were eligible to participate in the study if they had entered care before their 16th birthday, were still in care at age 17, and had been removed from home for reasons other than delinquency. Baseline survey data were collected from 732 study participants when they were 17 or 18 years old. Study participants were re-interviewed at ages 19 (n = 603), 21 (n = 591), and 23 or 24 (n = 602). A fifth wave of survey data will be collected when study participants are 25 or 26 years old.Because many of the questions Midwest Study participants were also asked as part of the National Longitudinal Study of Adolescent Health, it is possible to make comparisons between this sample of former foster youth and a nationally representative sample of young people in the general population. These comparisons indicate that young people who have aged out of foster care are faring poorly as a group relative to their peers across a variety of domains.The Midwest Study also presents a unique opportunity to compare the outcomes of young people from one state (i.e., Illinois) that allows foster youth to remain in care until their 21st birthday to the outcomes of young people from two other states (i.e., Iowa and Wisconsin) in which foster youth generally age out when they are 18 years old. The data suggest that extending foster care until age 21 may be associated with better outcomes, at least in some domains

    Midwest Evaluation of the Adult Functioning of Former Foster Youth: outcomes at age 21

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    The Midwest Evaluation of the Adult Functioning of Former Foster Youth (Midwest Study) is a longitudinal study that has been following a sample of young people from Iowa, Wisconsin, and Illinois as they transition out of foster care into adulthood. It is a collaborative effort involving Chapin Hall at the University of Chicago; the University of Wisconsin Survey Center; and the public child welfare agencies in Illinois, Iowa, and Wisconsin. This report concentrates on the outcomes of 21 year old youth as they age out of the child welfare system and transition to adulthood

    Snapshots of a protein folding intermediate

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    We have investigated the folding dynamics of Thermus thermophilus cytochrome c_(552) by time-resolved fluorescence energy transfer between the heme and each of seven site-specific fluorescent probes. We have found both an equilibrium unfolding intermediate and a distinct refolding intermediate from kinetics studies. Depending on the protein region monitored, we observed either two-state or three-state denaturation transitions. The unfolding intermediate associated with three-state folding exhibited native contacts in β-sheet and C-terminal helix regions. We probed the formation of a refolding intermediate by time-resolved fluorescence energy transfer between residue 110 and the heme using a continuous flow mixer. The intermediate ensemble, a heterogeneous mixture of compact and extended polypeptides, forms in a millisecond, substantially slower than the ∼100-μs formation of a burst-phase intermediate in cytochrome c. The surprising finding is that, unlike for cytochrome c, there is an observable folding intermediate, but no microsecond burst phase in the folding kinetics of the structurally related thermostable protein

    Structural Control of ^1A_(2u)-to-^3A_(2u) Intersystem Crossing in Diplatinum(II,II) Complexes

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    Analysis of variable-temperature fluorescence quantum yield and lifetime data for per(difluoroboro)tetrakis(pyrophosphito)diplatinate(II) ([Pt_2(μ-P_2O_5(BF_2)_(2)4)]^(4–), abbreviated Pt(pop-BF_2)), yields a radiative decay rate (k_r = 1.7 × 10^8 s^(–1)) an order of magnitude greater than that of the parent complex, Pt(pop). Its temperature-independent and activated intersystem crossing (ISC) pathways are at least 18 and 142 times slower than those of Pt(pop) [ISC activation energies: 2230 cm^(–1) for Pt(pop-BF_2); 1190 cm^(–1) for Pt(pop)]. The slowdown in the temperature-independent ISC channel is attributed to two factors: (1) reduced spin–orbit coupling between the ^1A_(2u) state and the mediating triplet(s), owing to increases of LMCT energies relative to the excited singlet; and (2) diminished access to solvent, which for Pt(pop) facilitates dissipation of the excess energy into solvent vibrational modes. The dramatic increase in E_a is attributed to increased P-O-P framework rigidity, which impedes symmetry-lowering distortions, in particular asymmetric vibrations in the Pt_2(P-O-P)_4 core that would allow direct ^1A_(2u)–^3A_(2u) spin–orbit coupling

    Psychological stress in adolescent and adult mice increases neuroinflammation and attenuates the response to LPS challenge

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    <p>Abstract</p> <p>Background</p> <p>There is ample evidence that psychological stress adversely affects many diseases. Recent evidence has shown that intense stressors can increase inflammation within the brain, a known mediator of many diseases. However, long-term outcomes of chronic psychological stressors that elicit a neuroinflammatory response remain unknown.</p> <p>Methods</p> <p>To address this, we have modified previously described models of rat/mouse predatory stress (PS) to increase the intensity of the interaction. We postulated that these modifications would enhance the predator-prey experience and increase neuroinflammation and behavioral dysfunction in prey animals. In addition, another group of mice were subjected to a modified version of chronic unpredictable stress (CUS), an often-used model of chronic stress that utilizes a combination of stressors that include physical, psychological, chemical, and other. The CUS model has been shown to exacerbate a number of inflammatory-related diseases via an unknown mechanism. Using these two models we sought to determine: 1) whether chronic PS or CUS modulated the inflammatory response as a proposed mechanism by which behavioral deficits might be mediated, and 2) whether chronic exposure to a pure psychological stressor (PS) leads to deficits similar to those produced by a CUS model containing psychological and physical stressors. Finally, to determine whether acute PS has neuroinflammatory consequences, adult mice were examined at various time-points after PS for changes in inflammation.</p> <p>Results</p> <p>Adolescent mice subjected to chronic PS had increased basal expression of inflammation within the midbrain. CUS and chronic PS mice also had an impaired inflammatory response to a subsequent lipopolysaccharide challenge and PS mice displayed increased anxiety- and depressive-like behaviors following chronic stress. Finally, adult mice subjected to acute predatory stress had increased gene expression of inflammatory factors.</p> <p>Conclusion</p> <p>Our results demonstrate that predatory stress, an ethologically relevant stressor, can elicit changes in neuroinflammation and behavior. The predatory stress model may be useful in elucidating mechanisms by which psychological stress modulates diseases with an inflammatory component.</p

    Genetic diversity fuels gene discovery for tobacco and alcohol use

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    Tobacco and alcohol use are heritable behaviours associated with 15% and 5.3% of worldwide deaths, respectively, due largely to broad increased risk for disease and injury(1-4). These substances are used across the globe, yet genome-wide association studies have focused largely on individuals of European ancestries(5). Here we leveraged global genetic diversity across 3.4 million individuals from four major clines of global ancestry (approximately 21% non-European) to power the discovery and fine-mapping of genomic loci associated with tobacco and alcohol use, to inform function of these loci via ancestry-aware transcriptome-wide association studies, and to evaluate the genetic architecture and predictive power of polygenic risk within and across populations. We found that increases in sample size and genetic diversity improved locus identification and fine-mapping resolution, and that a large majority of the 3,823 associated variants (from 2,143 loci) showed consistent effect sizes across ancestry dimensions. However, polygenic risk scores developed in one ancestry performed poorly in others, highlighting the continued need to increase sample sizes of diverse ancestries to realize any potential benefit of polygenic prediction.Peer reviewe

    The diversity and evolution of pollination systems in large plant clades: Apocynaceae as a case study

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    Background and Aims Large clades of angiosperms are often characterized by diverse interactions with pollinators, but how these pollination systems are structured phylogenetically and biogeographically is still uncertain for most families. Apocynaceae is a clade of >5300 species with a worldwide distribution. A database representing >10 % of species in the family was used to explore the diversity of pollinators and evolutionary shifts in pollination systems across major clades and regions. Methods The database was compiled from published and unpublished reports. Plants were categorized into broad pollination systems and then subdivided to include bimodal systems. These were mapped against the five major divisions of the family, and against the smaller clades. Finally, pollination systems were mapped onto a phylogenetic reconstruction that included those species for which sequence data are available, and transition rates between pollination systems were calculated. Key Results Most Apocynaceae are insect pollinated with few records of bird pollination. Almost three-quarters of species are pollinated by a single higher taxon (e.g. flies or moths); 7 % have bimodal pollination systems, whilst the remaining approx. 20 % are insect generalists. The less phenotypically specialized flowers of the Rauvolfioids are pollinated by a more restricted set of pollinators than are more complex flowers within the Apocynoids + Periplocoideae + Secamonoideae + Asclepiadoideae (APSA) clade. Certain combinations of bimodal pollination systems are more common than others. Some pollination systems are missing from particular regions, whilst others are over-represented. Conclusions Within Apocynaceae, interactions with pollinators are highly structured both phylogenetically and biogeographically. Variation in transition rates between pollination systems suggest constraints on their evolution, whereas regional differences point to environmental effects such as filtering of certain pollinators from habitats. This is the most extensive analysis of its type so far attempted and gives important insights into the diversity and evolution of pollination systems in large clades

    The impact of breastfeeding patterns on regional differences in infant mortality in Germany, 1910

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    This paper examines the impact of breastfeeding practices on the large regional differences in infant mortality in Germany around 1910. Breastfeeding is strongly negatively associated with infant mortality and remains so after controlling for public health measures and for demographic, economic, and social factors that also affect infant mortality. But it contributes much less to regional differences in infant mortality than do access to medical care, percentage illegitimate and marital fertility. Breastfeeding is less important than these other factors because it affects fewer causes of death and has a smaller impact on cause-specific infant mortality rates. L'auteur étudie l'impact des pratiques d'allaitement sur les grandes différences régionales de mortalité infantile observées en Allemagne aux alentours de 1910. Il existe une association fortement négative entre l'allaitement et la mortalité infantile, même quand on contrôle les facteurs démographiques, économiques, sociaux et de politique sanitaire, qui, eux aussi, affectent la mortalité infantile. Mais les différences régionales de mortalité infantile s'expliquent nettement moins par l'allaitement que par l'accessibilité des soins médicaux, le taux d'illégitimité des naissances et la fécondité légitime. L'allaitement est un facteur de moindre importance que ceux-ci parce qu'il n'a d'impact que sur un petit nombre de causes de décès, et un faible impact sur les taux de mortalité infantile par cause.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42730/1/10680_2005_Article_BF01796777.pd

    Delineating the molecular and phenotypic spectrum of the SETD1B-related syndrome

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    Purpose: Pathogenic variants in SETD1B have been associated with a syndromic neurodevelopmental disorder including intellectual disability, language delay, and seizures. To date, clinical features have been described for 11 patients with (likely) pathogenic SETD1B sequence variants. This study aims to further delineate the spectrum of the SETD1B-related syndrome based on characterizing an expanded patient cohort. Methods: We perform an in-depth clinical characterization of a cohort of 36 unpublished individuals with SETD1B sequence variants, describing their molecular and phenotypic spectrum. Selected variants were functionally tested using in vitro and genome-wide methylation assays. Results: Our data present evidence for a loss-of-function mechanism of SETD1B variants, resulting in a core clinical phenotype of global developmental delay, language delay including regression, intellectual disability, autism and other behavioral issues, and variable epilepsy phenotypes. Developmental delay appeared to precede seizure onset, suggesting SETD1B dysfunction impacts physiological neurodevelopment even in the absence of epileptic activity. Males are significantly overrepresented and more severely affected, and we speculate that sex-linked traits could affect susceptibility to penetrance and the clinical spectrum of SETD1B variants. Conclusion: Insights from this extensive cohort will facilitate the counseling regarding the molecular and phenotypic landscape of newly diagnosed patients with the SETD1B-related syndrome
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