70 research outputs found

    Localization of the thyrotropin-releasing hormone gene, Trh , on mouse Chromosome 6

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47026/1/335_2004_Article_BF00355651.pd

    Fire and the relative roles of weather, climate and landscape characteristics in the Great Lakes-St. Lawrence forest of Canada

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    Question: In deciduous-dominated forest landscapes, what are the relative roles of fire weather, climate, human and biophysical landscape characteristics for explaining variation in large fire occurrence and area burned? Location: The Great Lakes-St. Lawrence forest of Canada. Methods: We characterized the recent (1959-1999) regime of large (≥ 200 ha) fires in 26 deciduous-dominated landscapes and analysed these data in an information-theoretic framework to compare six hypotheses that related fire occurrence and area burned to fire weather severity, climate normals, population and road densities, and enduring landscape characteristics such as surficial deposits and large lakes. Results: 392 large fires burned 833 698 ha during the study period, annually burning on average 0.07% ± 0.42% of forested area in each landscape. Fire activity was strongly seasonal, with most fires and area burned occurring in May and June. A combination of antecedent-winter precipitation, fire season precipitation deficit/surplus and percent of landscape covered by well-drained surficial deposits best explained fire occurrence and area burned. Fire occurrence varied only as a function of fire weather and climate variables, whereas area burned was also explained by percent cover of aspen and pine stands, human population density and two enduring characteristics: percent cover of large water bodies and glaciofluvial deposits. Conclusion: Understanding the relative role of these variables may help design adaptation strategies for forecasted increases in fire weather severity by allowing (1) prioritization of landscapes according to enduring characteristics and (2) management of their composition so that substantially increased fire activity would be necessary to transform landscape structure and composition

    Genes for tesin, villin and desmin are linked on mouse Chromosome 1

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47016/1/335_2004_Article_BF00354299.pd

    Chromosomal localization of the large subunit of mouse replication factor C in the mouse and human

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47015/1/335_2004_Article_BF00350900.pd

    Synaptotagmin genes on mouse Chromosomes 1, 7, and 10 and human Chromosome 19

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47020/1/335_2004_Article_BF00293017.pd

    Localization of the murine cholecystokinin A and B receptor genes

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    We have determined the chromosomal locations of the two cholecystokinin (CCK) receptor genes in the mouse. Genetic localization utilized an interspecific backcross panel formed from the cross (C57BL/6J x Mus spretus ) F 1 x Mus spretus . Genomic DNAs from 94 individuals in the backcross were analyzed by Southern hybridization with rat CCK A and CCK B receptor cDNA probes. Unique map positions were determined by haplotype analysis with 650 previously mapped loci in the mouse backcross. The CCK A receptor gene ( Cckar ) mapped to mouse Chromosome (Chr) 5, in tight linkage with the DNA marker D5Bir8 . The CCK B receptor gene ( Cckbr ) mapped to mouse Chr 7, tightly linked to the β-hemoglobin locus ( Hbb ). This localization places Cckbr in the same region as the mouse obesity mutation tubby ( tub ), which also maps near Hbb (2.4±1.4 cM). Since CCK can function as a satiety factor when administered to rodents, localization of Cckbr near the tub mutation identifies this receptor as a possible candidate gene for this obesity mutation.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47021/1/335_2004_Article_BF00352408.pd

    Truncating SRCAP variants outside the Floating-Harbor syndrome locus cause a distinct neurodevelopmental disorder with a specific DNA methylation signature

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    Truncating variants in exons 33 and 34 of the SNF2-related CREBBP activator protein (SRCAP) gene cause the neurodevelopmental disorder (NDD) Floating-Harbor syndrome (FLHS), characterized by short stature, speech delay, and facial dysmorphism. Here, we present a cohort of 33 individuals with clinical features distinct from FLHS and truncating (mostly de novo) SRCAP variants either proximal (n = 28) or distal (n = 5) to the FLHS locus. Detailed clinical characterization of the proximal SRCAP individuals identified shared characteristics: developmental delay with or without intellectual disability, behavioral and psychiatric problems, non-specific facial features, musculoskeletal issues, and hypotonia. Because FLHS is known to be associated with a unique set of DNA methylation (DNAm) changes in blood, a DNAm signature, we investigated whether there was a distinct signature associated with our affected individuals. A machine-learning model, based on the FLHS DNAm signature, negatively classified all our tested subjects. Comparing proximal variants with typically developing controls, we identified a DNAm signature distinct from the FLHS signature. Based on the DNAm and clinical data, we refer to the condition as "non-FLHS SRCAP-related NDD.'' All five distal variants classified negatively using the FLHS DNAm model while two classified positively using the proximal model. This suggests divergent pathogenicity of these variants, though clinically the distal group presented with NDD, similar to the proximal SRCAP group. In summary, for SRCAP, there is a clear relationship between variant location, DNAm profile, and clinical phenotype. These results highlight the power of combined epigenetic, molecular, and clinical studies to identify and characterize genotype-epigenotype-phenotype correlations.Genetics of disease, diagnosis and treatmen

    Private financing in urban public schools: Inequalities in a stratified education marketplace

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    This study examines inequalities of school funding as exclusively generated by the parent community in urban public schools, and potentially illuminates a secondary impact of between-school segregation. For schools that are largely understood as free, the substantial injections of private financing into public schools indicate a concerning tension for fairness and equity. Using a census dataset of all public schools in one Australian capital city (n = 150), we compare reported parent ‘contributions, fees and charges’ and how they are patterned by measures of school disadvantage and advantage. We found a statistically significant relationship between private financing and measures of school-based advantage or disadvantage, over a four-year period. Advantaged schools generate up to six times greater income in comparison to disadvantaged schools over a four-year period, and we argue that the substantial gaps function as another form of ‘compounded disadvantage’ for residualised public schools and a tiered effect of segregation

    Inequalities in the private funding of public schools: Parent financial contributions and school socioeconomic status

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    Parent involvement in their child’s schooling is routinely celebrated and emphasised in government education policy in many countries. We take a critical lens to examining parent involvement by investigating voluntary parent fees in public secondary schools, and how these fees are patterned by school socioeconomic status (SES). In Australia, where this study is located, public schools may request ‘voluntary’ fees from parents to enhance education programmes and facilities. As public schools are increasingly situated in a competitive market, this has arguably augmented pressure for schools and their communities to generate funds. Our findings show large inequalities between public schools, with high-SES schools enjoying more than four times parent-generated income than low-SES schools. Parent financial contributions are a form of structural inequality that benefits socially advantaged students and schools, potentially serving as both a cause and consequence of socially segregated schooling. We conclude with recommendations for policy

    School segregation: Theoretical insights and future directions

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    School segregation is both an enduring and growing area of research interest. School segregation is shaped by multiple and complex forces within educational ecosystems, including individual students and households, education jurisdictions, organisational (dis)incentives, policies, and larger societal characteristics and contexts. As a field of study, comparative education emphasises the complex interactions of historical and socio-cultural context with actors, social institutions and policy settings for explaining educational phenomena. With this foundation, comparative education is uniquely positioned to integrate studies of school segregation into a comprehensive and comparative framework for deepening our theoretical understanding of school segregation and its causes, solutions, and impacts on educational equity. This paper introduces the special issue on school segregation. In addition to providing an overview of the special issue, we present a theoretical framework that may be useful for informing future comparative studies and conclude with several possible future research directions
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