2,497 research outputs found
Establishing a Center to Support Faculty Research
This is the author's accepted manuscript. The original publication is available at http://dx.doi.org/10.1007/s10755-005-8347-z.This article describes the establishment in fall 2002 of a School of Education Research Center designed to support faculty in increasing productivity and quality in research. Details are provided about center goals, services, staffing, space, resources, and logistics during the first year of operation. In addition, data are shared about faculty usage of the Center, the level of faculty satisfaction with center services in the first year, and initial increases in faculty productivity. The article concludes with plans for continued data collection to monitor the impact of the Center, a discussion of lessons learned at this point in the Center's development, and possibilities for the evolution of the Center
Predictors of rater bias in the assessment of social-emotional competence
The Devereux Student Strengths Assessment Mini (DESSA-Mini) (LeBuffe, Shapiro, &
Naglieri, 2014) efficiently monitors the growth of Social-Emotional Competence (SEC)
in the routine implementation of Social Emotional Learning programs. The DESSAMini
is used to assess approximately half a million children around the world. Since
behavior rating scales can have ârater biasâ, this paper examines rater characteristics that
contribute to DESSA-Mini ratings. Rater characteristics and DESSA-Mini ratings were
collected from elementary school classroom teachers (n=72) implementing TOOLBOX
in a racially/ethnically diverse California school district. Teachers rated 1,676 students,
who scored similarly to a national reference group. Multilevel modeling analysis showed
that only 16% of variance in DESSA-mini ratings was attributable to raters.
Relationships between teacher characteristics and ratings were estimated to examine
rater variance. Collectively, four characteristics of teachers (perceived barriers to student
learning, sense of their âtypicalâ studentâs level of SEC, anticipation of SEL program
implementation challenges, and intentions to fully implement a newly adopted SEL
program) accounted for bias in teacher-generated DESSA scores, leaving only 10% of
the variance unexplained. Identified sources of ârater biasâ can be controlled for in
research and addressed through thoughtful program selection, training, and
implementation.peer-reviewe
Teachersâ assessment of âimplementation leadershipâ during a new social emotional learning initiative
Pathways through Adolescenc
ILâ17A deficiency mitigates bleomycinâinduced complement activation during lung fibrosis
Interleukin 17A (ILâ17A) and complement (CâČ) activation have each been implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF). We have reported that ILâ17A induces epithelial injury via TGFâÎČ in murine bronchiolitis obliterans; that TGFâÎČ and the CâČ cascade present signaling interactions in mediating epithelial injury; and that the blockade of CâČ receptors mitigates lung fibrosis. In the present study, we investigated the role of ILâ17A in regulating CâČ in lung fibrosis. Microarray analyses of mRNA isolated from primary normal human small airway epithelial cells indicated that ILâ17A (100 ng/ml; 24 h; n = 5 donor lungs) induces CâČ components (CâČ factor B, C3, and GPCR kinase isoform 5), cytokines (IL8, â6, and â1B), and cytokine ligands (CXCL1, â2, â3, â5, â6, and â16). ILâ17A induces protein and mRNA regulation of CâČ components and the synthesis of active CâČ 3a (C3a) in normal primary human alveolar type II epithelial cells (AECs). Wildâtype mice subjected to ILâ17A neutralization and ILâ17A knockout (i717aâ/â) mice were protected against bleomycin (BLEO)âinduced fibrosis and collagen deposition. Further, BLEOâinjured i17aâ/â mice had diminished levels of circulating Krebs Von Den Lungen 6 (alveolar epithelial injury marker), local caspaseâ3/7, and local endoplasmic reticular stressârelated genes. BLEOâinduced local CâČ activation [C3a, C5a, and terminal CâČ complex (C5bâ9)] was attenuated in il17aâ/â mice, and ILâ17A neutralization prevented the loss of epithelial CâČ inhibitors (CâČ receptorâ1 related isoform Y and decay accelerating factor), and an increase in local TUNEL levels. RNAiâmediated gene silencing of il17a in fibrotic mice arrested the progression of lung fibrosis, attenuated cellular apoptosis (caspaseâ3/7) and lung deposition of collagen and CâČ (C5bâ9). Compared to normals, plasma from IPF patients showed significantly higher hemolytic activity. Our findings demonstrate that limiting complement activation by neutralizing ILâ17A is a potential mechanism in ameliorating lung fibrosis.âCipolla, E., Fisher, A. J., Gu, H., Mickler, E. A., Agarwal, M., Wilke, C. A., Kim, K. K., Moore, B. B., Vittal, R. ILâ17A deficiency mitigates bleomycinâinduced complement activation during lung fibrosis. FASEB J. 31, 5543â5556 (2017). www.fasebj.orgPeer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/154482/1/fsb2fj201700289r-sup-0001.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/154482/2/fsb2fj201700289r.pd
On classical super-radiance in Kerr-Newman-anti-de Sitter black holes
We study in detail the modes of a classical scalar field on a
Kerr-Newman-anti-de Sitter (KN-AdS) black hole. We construct sets of basis
modes appropriate to the two possible boundary conditions (``reflective'' and
``transparent'') at time-like infinity, and consider whether super-radiance is
possible. If we employ ``reflective'' boundary conditions, all modes are
non-super-radiant. On the other hand, for ``transparent'' boundary conditions,
the presence of super-radiance depends on our definition of positive frequency.
For those KN-AdS black holes having a globally time-like Killing vector, the
natural choice of positive frequency leads to no super-radiance. For other
KN-AdS black holes, there is a choice of positive frequency which gives no
super-radiance, but for other choices there will, in general, be
super-radiance.Comment: 23 pages, 3 figures, v2: minor changes, references adde
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EM-mosaic detects mosaic point mutations that contribute to congenital heart disease.
BackgroundThe contribution of somatic mosaicism, or genetic mutations arising after oocyte fertilization, to congenital heart disease (CHD) is not well understood. Further, the relationship between mosaicism in blood and cardiovascular tissue has not been determined.MethodsWe developed a new computational method, EM-mosaic (Expectation-Maximization-based detection of mosaicism), to analyze mosaicism in exome sequences derived primarily from blood DNA of 2530 CHD proband-parent trios. To optimize this method, we measured mosaic detection power as a function of sequencing depth. In parallel, we analyzed our cohort using MosaicHunter, a Bayesian genotyping algorithm-based mosaic detection tool, and compared the two methods. The accuracy of these mosaic variant detection algorithms was assessed using an independent resequencing method. We then applied both methods to detect mosaicism in cardiac tissue-derived exome sequences of 66 participants for which matched blood and heart tissue was available.ResultsEM-mosaic detected 326 mosaic mutations in blood and/or cardiac tissue DNA. Of the 309 detected in blood DNA, 85/97 (88%) tested were independently confirmed, while 7/17 (41%) candidates of 17 detected in cardiac tissue were confirmed. MosaicHunter detected an additional 64 mosaics, of which 23/46 (50%) among 58 candidates from blood and 4/6 (67%) of 6 candidates from cardiac tissue confirmed. Twenty-five mosaic variants altered CHD-risk genes, affecting 1% of our cohort. Of these 25, 22/22 candidates tested were confirmed. Variants predicted as damaging had higher variant allele fraction than benign variants, suggesting a role in CHD. The estimated true frequency of mosaic variants above 10% mosaicism was 0.14/person in blood and 0.21/person in cardiac tissue. Analysis of 66 individuals with matched cardiac tissue available revealed both tissue-specific and shared mosaicism, with shared mosaics generally having higher allele fraction.ConclusionsWe estimate that ~â1% of CHD probands have a mosaic variant detectable in blood that could contribute to cardiac malformations, particularly those damaging variants with relatively higher allele fraction. Although blood is a readily available DNA source, cardiac tissues analyzed contributed ~â5% of somatic mosaic variants identified, indicating the value of tissue mosaicism analyses
Dietary betaine supplementation increases Fgf21 levels to improve glucose homeostasis and reduce hepatic lipid accumulation in mice
Identifying markers of human insulin resistance may permit development of new approaches for treatment and prevention of type 2 diabetes. To this end, we analyzed the fasting plasma metabolome in metabolically characterized human volunteers across a spectrum of insulin resistance. We demonstrate that plasma betaine levels are reduced in insulin-resistant humans and correlate closely with insulin sensitivity. Moreover, betaine administration to mice with diet-induced obesity prevents the development of impaired glucose homeostasis, reduces hepatic lipid accumulation, increases white adipose oxidative capacity, and enhances whole-body energy expenditure. In parallel with these beneficial metabolic effects, betaine supplementation robustly increased hepatic and circulating fibroblast growth factor (Fgf)21 levels. Betaine administration failed to improve glucose homeostasis and liver fat content in Fgf21(-/-) mice, demonstrating that Fgf21 is necessary for betaine's beneficial effects. Together, these data indicate that dietary betaine increases Fgf21 levels to improve metabolic health in mice and suggest that betaine supplementation merits further investigation as a supplement for treatment or prevention of type 2 diabetes in humans
TGF-b2 induction regulates invasiveness of theileria-transformed leukocytes and disease susceptibility
Theileria parasites invade and transform bovine leukocytes causing either East Coast fever (T. parva), or tropical theileriosis (T. annulata). Susceptible animals usually die within weeks of infection, but indigenous infected cattle show markedly reduced pathology, suggesting that host genetic factors may cause disease susceptibility. Attenuated live vaccines are widely used to control tropical theileriosis and attenuation is associated with reduced invasiveness of infected macrophages in vitro. Disease pathogenesis is therefore linked to aggressive invasiveness, rather than uncontrolled proliferation of Theileria-infected leukocytes. We show that the invasive potential of Theileria-transformed leukocytes involves TGF-b signalling. Attenuated live vaccine lines express reduced TGF-b2 and their invasiveness can be rescued with exogenous TGF-b. Importantly, infected macrophages from disease susceptible Holstein-Friesian (HF) cows express more TGF-b2 and traverse Matrigel with great efficiency compared to those from disease-resistant Sahiwal cattle. Thus, TGF-b2 levels correlate with disease susceptibility. Using fluorescence and time-lapse video microscopy we show that Theileria-infected, disease-susceptible HF macrophages exhibit increased actin dynamics in their lamellipodia and podosomal adhesion structures and develop more membrane blebs. TGF-b2-associated invasiveness in HF macrophages has a transcription-independent element that relies on cytoskeleton remodelling via activation of Rho kinase (ROCK). We propose that a TGF-b autocrine loop confers an amoeboid-like motility on Theileria-infected leukocytes, which combines with MMP-dependent motility to drive invasiveness and virulence
TIA1 Mutations in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia Promote Phase Separation and Alter Stress Granule Dynamics.
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are age-related neurodegenerative disorders with shared genetic etiologies and overlapping clinical and pathological features. Here we studied a novel ALS/FTD family and identified the P362L mutation in the low-complexity domain (LCD) of T cell-restricted intracellular antigen-1 (TIA1). Subsequent genetic association analyses showed an increased burden of TIA1 LCD mutations in ALS patients compared to controls (p = 8.7 Ă 1
Measurement of the Lifetime Difference Between B_s Mass Eigenstates
We present measurements of the lifetimes and polarization amplitudes for B_s
--> J/psi phi and B_d --> J/psi K*0 decays. Lifetimes of the heavy (H) and
light (L) mass eigenstates in the B_s system are separately measured for the
first time by determining the relative contributions of amplitudes with
definite CP as a function of the decay time. Using 203 +/- 15 B_s decays, we
obtain tau_L = (1.05 +{0.16}/-{0.13} +/- 0.02) ps and tau_H = (2.07
+{0.58}/-{0.46} +/- 0.03) ps. Expressed in terms of the difference DeltaGamma_s
and average Gamma_s, of the decay rates of the two eigenstates, the results are
DeltaGamma_s/Gamma_s = (65 +{25}/-{33} +/- 1)%, and DeltaGamma_s = (0.47
+{0.19}/-{0.24} +/- 0.01) inverse ps.Comment: 8 pages, 3 figures, 2 tables; as published in Physical Review Letters
on 16 March 2005; revisions are for length and typesetting only, no changes
in results or conclusion
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