bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evidence of a latitudinal gradient in spider diversity in Australian cotton
Authors: WHITEHOUSE MARY E. A. , HARDWICK SCOTT , SCHOLZ BRAD C. G. , ANNELLS AMANDA J. , WARD ANDREW , GRUNDY PAUL R. , HARDEN STEVEN 
Published: January 2009

AbstractThe most common explanation for species diversity increasing towards the tropics is the corresponding increase in habitats (spatial heterogeneity). Consequently, a monoculture (like cotton in Australia) which is grown along a latitudinal gradient, should have the same degree of species diversity throughout its range. We tested to see if diversity in a dominant cotton community (spiders) changed with latitude, and if the community was structurally identical in different parts of Australia. We sampled seven sites extending over 20° of latitude. At each site we sampled 1–3 fields 3–5 times during the cotton growing season using pitfall traps and beatsheets, recording all the spiders collected to family. We found that spider communities in cotton are diverse, including a large range of foraging guilds, making them suitable for a conservation biological control programme. We also found that spider diversity increased from high to low latitudes, and the communities were different, even though the spiders were in the same monocultural habitat. Spider beatsheet communities around Australia were dominated by different families, and responded differently to seasonal changes, indicating that different pest groups would be targeted at different locations. These results show that diversity can increase from high to low latitudes, even if spatial heterogeneity is held constant, and that other factors external to the cotton crop are influencing spider species composition. Other models which may account for the latitudinal gradient, such as non‐equilibrium regional processes, are discussed.
Native Australian frogs avoid the scent of invasive cane toads
Authors: PIZZATTO LÍGIA , SHINE RICHARD 
Published: January 2009

AbstractInvasive species can affect the ecosystems they colonize by modifying the behaviour of native taxa; for example, avoidance of chemical cues from the invader may modify habitat use (shelter site selection) by native species. In laboratory trials, we show that metamorphs of most (but not all) native frog species on a tropical Australian floodplain avoid the scent of invasive cane toads (Bufo marinus Linnaeus 1758). Cane toads also avoid conspecific scent. This response might reduce vulnerability of metamorph frogs and toads to larger predatory toads. However, similar avoidance of one type of pungency control (garlic), and the presence of this avoidance behaviour in frogs at the toad invasion front (and hence, with no prior exposure to toads), suggest that this may not be an evolved toad‐specific response. Instead, our data support the simpler hypothesis that the metamorph anurans tend to avoid shelter sites that contain strong and unfamiliar scents. Temporal and spatial differences in activity of frogs versus toads, plus the abundance of suitable retreat sites during the wet season (the primary time of frog activity), suggest that avoiding toad scent will have only a minor impact on the behaviour of native frogs. However, this behavioural impact may be important when environmental conditions bring toads and frogs into closer contact.
The big ecological questions inhibiting effective environmental management in Australia
Authors: MORTON S. R. , HOEGH‐GULDBERG O. , LINDENMAYER D. B. , OLSON M. HARRISS , HUGHES L. , McCULLOCH M. T. , McINTYRE S. , NIX H. A. , PROBER S. M. , SAUNDERS D. A. , ANDERSEN A. N. , BURGMAN M. A. , LEFROY E. C. , LONSDALE W. M. , LOWE I. , McMICHAEL A. J. , PARSLOW J. S. , STEFFEN W. , WILLIAMS J. E. , WOINARSKI J. C. Z. 
Published: January 2009

AbstractThe need to improve environmental management in Australia is urgent because human health, well‐being and social stability all depend ultimately on maintenance of life‐supporting ecological processes. Ecological science can inform this effort, but when issues are socially and economically complex the inclination is to wait for science to provide answers before acting. Increasingly, managers and policy‐makers will be called on to use the present state of scientific knowledge to supply reasonable inferences for action based on imperfect knowledge. Hence, one challenge is to use existing ecological knowledge more effectively; a second is to tackle the critical unanswered ecological questions. This paper identifies areas of environmental management that are profoundly hindered by an inability of science to answer basic questions, in contrast to those areas where knowledge is not the major barrier to policy development and management. Of the 22 big questions identified herein, more than half are directly related to climate change. Several of the questions concern our limited understanding of the dynamics of marine systems. There is enough information already available to develop effective policy and management to address several significant ecological issues. We urge ecologists to make better use of existing knowledge in dialogue with policy‐makers and land managers. Because the challenges are enormous, ecologists will increasingly be engaging a wide range of other disciplines to help identify pathways towards a sustainable future.
Three microsatellites from the T1DGC MHC data set show highly significant association with type 1 diabetes, independent of the HLA‐DRB1, ‐DQA1 and ‐DQB1 genes
Authors: Eike M. C. , Humphreys K. , Becker T. , Olsson M. , Lie B. A. ,   Diabetes Genetics Consortium
Published: January 2009

Aim:  The aim of this study was to test the microsatellites in the Type 1 Diabetes Genetics Consortium major histocompatibility complex (MHC) data set for association with type 1 diabetes (T1D) independent of the HLA‐DRB1, ‐DQA1 and ‐DQB1 genes.Methods:  The data set was edited to contain only one affected child per family, and broad ethnic subgroups were defined. Genotypes for HLA‐DRB1, ‐DQA1 and ‐DQB1 were replaced by a haplotype code spanning all three loci, with phase inferred based on common haplotypes. The final data set contained 8190 samples in 2301 families, 59 microsatellites and the DRB1–DQA1–DQB1 haplotype code. Statistical analyses consisted of conditional logistic regression and haplotype estimations and linkage disequilibrium calculations.Results:  The data set was screened using a main effects test approach adjusted for DRB1–DQA1–DQB1, and significant results tested for validity. After these procedures, four markers remained significant at the Bonferroni‐corrected threshold: D6S2773 (p = 0.00014), DG6S185 (p = 0.00015), DG6S398 (p = 0.00043) and D6S2998 (p = 0.00015). These results were supported by allelic tests conditioned on DRB1–DQA1–DQB1 haplotypes, except for DG6S185, which may contain artefacts.Conclusions:  We have identified three microsatellites that mark additional risk factors for T1D at highly significant levels in the MHC. Further analyses are needed to establish the relationship with other possible genetic determinants in this region.
Several loci in the HLA class III region are associated with T1D risk after adjusting for DRB1‐DQB1
Authors: Valdes A. M. , Thomson G. ,   Diabetes Genetics Consortium
Published: January 2009

Aim:  Several studies have indicated that genes in the human leucocyte antigen (HLA) region additional to the HLA class II DRB1‐DQB1 contribute to type 1 diabetes (T1D) susceptibility. The aim of this study was to assess if markers in the class III Major Histocompatibility Complex (MHC) region are associated with T1D after accounting for linkage disequilibrium (LD) with DRB1‐DQB1.Methods:  We investigated 356 single nucleotide polymorphisms (SNPs) in the class III region covering 1.1 megabases in two subsets of data: 289 Human Biological Data Interchange (HBDI) Caucasian families and 597 additional Caucasian families collected by the Type 1 Diabetes Genetics Consortium (T1DGC). Analysis conditioning on DRB1‐DQB1 was performed using the overall conditional genotype method.Results:  Thirteen SNPs replicated in both subsets of the data and showed evidence of an additional effect on disease risk. Although some of the SNPs are in tight LD with each other, at least six of the associations were not because of LD with other class III markers. The strongest association within class III markers was with rs2395106 that maps 5′ to the NOTCH4 gene, which has also been implicated in susceptibility to rheumatoid arthritis. The second association was with rs707915 mapping to the MSH5 gene, in a block of six markers significantly associated with T1D after adjusting for LD with DR‐DQ. In total, six‐independent associations within class III were observed although results were not adjusted for LD with class I.Conclusions:  Our data confirm that the class III region is involved in T1D susceptibility and suggest that more than one gene in the region is involved.
MHC–environment interactions leading to type 1 diabetes: feasibility of an analysis of HLA DR‐DQ alleles in relation to manifestation periods and dates of birth
Authors: Badenhoop K. , Kahles H. , Seidl C. , Kordonouri O. , Lopez E. R. , Walter M. , Rosinger S. , Ziegler A. , Böhm B. O. ,   Diabetes Genetics Consortium
Published: January 2009

Aim:  The region on chromosome 6p21 (IDDM1) confers the largest part of genetic susceptibility to type 1 diabetes (T1D) with particular human leucocyte antigen (HLA) alleles predisposing and others protecting from it. As T1D is primarily a “sporadic” disease, the pathophysiology must involve gene–environment interactions. We searched for indirect evidence for such major histocompatibility complex (MHC)–environment interactions by asking two questions: (i) can the degree of an HLA association vary over time periods? and (ii) if a prenatal event like an intrauterine infection – that might cluster in seasons – leads to differences of HLA associations in patients with particular birth months?Methods:  We screened the Type 1 Diabetes Genetics Consortium (T1DGC) database (in addition our own database and the original UK, US and SCAND databases) for MHC DR‐DQ and CTLA4 associations. First, we separated the groups of patients with onset of disease before 1980 in comparison with onset after 1980. Second, we analysed the data according to dates of birth (grouped in months). Not all patients’ dates of birth or manifestation periods were available, leading to different group sizes. There were 282 patients analysed for manifestation periods and 329 for birth month.Results:  The cohorts of manifestation before 1980 demonstrated a significantly lower frequency of DQ2/X (2 vs. 14.2%; p = 0.03). There was a trend for DQ8/x to be more frequent for manifestations before 1980 (34 vs. 21.6%; p < 0.10). Other alleles did not differ significantly. The months of birth were not evenly distributed. Significant deviations from the whole group were seen in August (DQ2/8 trough and DQx/x high), whereas birth in September was more frequent in DQ8/x or DQ8/8 carriers. This pattern was significantly different from the expected distribution of months at birth (13.9 vs. 7.6%; p < 0.04).Conclusions:  We demonstrate the feasibility of an analysis that searches for indirect evidence of gene–environment interactions. These preliminary data need to be confirmed in larger data sets.
Association of MHC SNP genotype with susceptibility to type 1 diabetes: a modified survival approach
Authors: McKinnon E. , Morahan G. , Nolan D. , James I. ,   Diabetes Genetics Consortium
Published: January 2009

Aim: The Major Histocompatibility Complex (MHC) is a highly polymorphic region on chromosome 6 encompassing the human leucocyte antigen (HLA)‐DQ/DRloci most predictive of susceptibility to type 1 diabetes (T1D). To assess the contribution of other MHC genes, in this exploratory analysis of Type 1 Diabetes Genetics Consortium (T1DGC) family data we characterize association between susceptibility and MHC single nucleotide polymorphism (SNP) genotype, with an emphasis on effects of genetic variation additional to carriage of predisposing or protective MHC haplotypes.Methods: We use Cox regression analyses of age of onset, stratified by family, to jointly test both linkage and association. Analysis is restricted to children from families having both affected and unaffected siblings and is conducted with and without adjustment for known HLA class I and II effects. Model fits provide scores for each individual that are based on estimates of the probability of being affected by the age of 35, given the individual’s SNP genotype. The mean within‐family variation in these scores provides a measure that closely reflects the relative size of the likelihood ratio test statistics, and their covariation provides a means of mapping patterns of association that incorporate both effect size and commonality of effect that is attributable to the strong linkage disequilibrium (LD) extending across the region.Results: Univariate analyses yielded strong associations with T1D susceptibility that are dominated by SNPs in the class IIHLA‐DR/DQregion but extend across the MHC. Similar effects are frequently observed across SNPs within multiple genes, sometimes spanning hundreds of kilobases. SNPs within a region at the telomeric end of the class II geneHLA‐DRAyielded significant associations with and without adjustment for carriage of the predictive DR3, DR4, DR2 and DR7 HLA haplotypes, and remained highly prominent in a secondary analysis that was restricted to 66 families in whom at least one of the affected siblings carried neither the DR3 nor DR4 haplotype.Conclusions: While many of the associations can be attributed to LD between the SNPs and the dominantHLA‐DRB/DQA/DQBloci, there is also evidence of additional modifying effects.
ESTIMATION, PREDICTION AND INFERENCE FOR THE LASSO RANDOM EFFECTS MODEL
Authors: Foster Scott D. , Verbyla Arūnas P. , Pitchford Wayne S. 
Published: January 2009

SummaryThe least absolute shrinkage and selection operator (LASSO) can be formulated as a random effects model with an associated variance parameter that can be estimated with other components of variance. In this paper, estimation of the variance parameters is performed by means of an approximation to the marginal likelihood of the observed outcomes. The approximation is based on an alternative but equivalent formulation of the LASSO random effects model. Predictions can be made using point summaries of the predictive distribution of the random effects given the data with the parameters set to their estimated values. The standard LASSO method uses the mode of this distribution as the predictor. It is not the only choice, and a number of other possibilities are defined and empirically assessed in this article. The predictive mode is competitive with the predictive mean (best predictor), but no single predictor performs best across in all situations. Inference for the LASSO random effects is performed using predictive probability statements, which are more appropriate under the random effects formulation than tests of hypothesis.
Classroom Composition, Childcare History and Social Development: Are Childcare Effects Disappearing or Spreading?
Authors: Belsky Jay 
Published: January 2009

AbstractCore findings of the ongoing National Institute of Child Health and Human Development study of early child care and youth development through the end of the primary‐school years are summarized, highlighting the fact that both positive effects of good quality care on cognitive‐linguistic‐academic functioning and negative effects of extensive exposure to childcare on social development dissipate over time. Results showing that more time spent in any type of care or in center‐based care in particular predict somewhat elevated levels of externalizing problems are given special attention and considered in light of new results from the early childhood longitudinal study showing that being in kindergarten classrooms comprised of many children with extensive childcare histories contributes to externalizing behavior over and above children's own personal childcare histories. Implications of these latter results for the study of childcare are considered, especially with respect to the meaning of evidence documenting apparently dissipating childcare effects.
Making the Most of Small Effects
Authors: Thompson Ross A. 
Published: January 2009

AbstractThe idea that classroom social ecologies are shaped by the aggregate effects of peers’ prior care experiences is provocative, even though the evidence is weak that this explains the small and diminishing effect of childcare experience in the National Institute of Child Health and Human Development study. Small effects may indeed be small effects, but students of early development should attend to the potential importance of group‐level influences on social and cognitive growth.
Macroeconomic Fluctuations and Bank Lending: Evidence for Germany and the Euro Area
Authors: Eickmeier Sandra , Worms Andreas , Hofmann Boris 
Published: January 2009

Abstract
This paper analyzes the dynamic response of loans to the private sector and of economic activity to aggregate supply, demand and monetary policy shocks in Germany and the euro area based on a standard macroeconomic VAR using sign restrictions to identify the structural shocks. The main results of this analysis are that (i) with the exception of the response to the supply shock in Germany, the response of loans to the three macroeconomic shocks is rather weak and in most cases insignificant; (ii) the 2000-05 credit slowdown and weak economic performance in Germany were primarily driven by adverse supply shocks; and (iii) the marked slowdown in credit creation in Germany over this period actually represents a realignment of the outstanding stock of loans with its deterministic level. In order to assess the role of bank lending in the transmission of macroeconomic shocks, we further perform counterfactual simulations and analyze the dynamic responses of German loan subaggregates in order to test the distributional implications of potential credit market frictions. These exercises do not indicate that credit market frictions play an amplifying role in the transmission of macroeconomic fluctuations.
A clinical study of Henoch‐Schönlein Purpura associated with malignancy
Authors: Mitsui H , Shibagaki N , Kawamura T , Matsue H , Shimada S 
Published: January 2009

AbstractBackground Malignancy has been reported as a causative factor of cutaneous vasculitis, although only two retrospective epidemiological studies have analysed the association between Henoch‐Schönlein purpura (HSP) and malignancy to date.Objective To analyse the association between adult HSP and malignancy.Methods We retrospectively reviewed the medical records of patients and found 103 cases of HSP over the past 20 years. Fifty‐three cases (aged ≥ 41 years) were categorized to two groups including ‘with malignancy’ or ‘without malignancy’, so that we could analyse the differences of clinical features between them. We also compared our study to previous reports.Results Twenty‐three cases out of 53 patients exhibited underlying malignant tumours. We focused on nine patients in which malignant tumours were thought to be strongly associated. Seven of nine patients exhibited new metastatic lesions or died due to underlying cancer within 1–32 months.Conclusions An association between HSP and malignant disease might have important diagnostic and pathophysiologic implications.Conflicts of interestNone declared
Is neurofeedback an efficacious treatment for ADHD? A randomised controlled clinical trial
Authors: Gevensleben Holger , Holl Birgit , Albrecht Björn , Vogel Claudia , Schlamp Dieter , Kratz Oliver , Studer Petra , Rothenberger Aribert , Moll Gunther H. , Heinrich Hartmut 
Published: January 2009

Background:  For children with attention deficit/hyperactivity disorder (ADHD), a reduction of inattention, impulsivity and hyperactivity by neurofeedback (NF) has been reported in several studies. But so far, unspecific training effects have not been adequately controlled for and/or studies do not provide sufficient statistical power. To overcome these methodological shortcomings we evaluated the clinical efficacy of neurofeedback in children with ADHD in a multisite randomised controlled study using a computerised attention skills training as a control condition.Methods:  102 children with ADHD, aged 8 to 12 years, participated in the study. Children performed either 36 sessions of NF training or a computerised attention skills training within two blocks of about four weeks each (randomised group assignment). The combined NF treatment consisted of one block of theta/beta training and one block of slow cortical potential (SCP) training. Pre‐training, intermediate and post‐training assessment encompassed several behaviour rating scales (e.g., the German ADHD rating scale, FBB‐HKS) completed by parents and teachers. Evaluation (‘placebo’) scales were applied to control for parental expectations and satisfaction with the treatment.Results:  For parent and teacher ratings, improvements in the NF group were superior to those of the control group. For the parent‐rated FBB‐HKS total score (primary outcome measure), the effect size was .60. Comparable effects were obtained for the two NF protocols (theta/beta training, SCP training). Parental attitude towards the treatment did not differ between NF and control group.Conclusions:  Superiority of the combined NF training indicates clinical efficacy of NF in children with ADHD. Future studies should further address the specificity of effects and how to optimise the benefit of NF as treatment module for ADHD.
X‐linked mental retardation: focus on synaptic function and plasticity
Authors: Humeau Yann , Gambino Frédéric , Chelly Jamel , Vitale Nicolas 
Published: January 2009

AbstractAmong mental disorders, mental retardation has been shown to be caused by various factors including a large array of genetic mutations. On the basis of remarkable progress, the emerging view is that defects in the regulation of synaptic activity and morphogenesis of dendritic spines are apparently common features associated with mutations in several genes implicated in mental retardation. In this review, we will discuss X‐linked MR‐related gene products that are potentially involved in the normal structure and function of the synapses, with a particular focus on pre‐ and/or post‐synaptic plasticity mechanisms. Progress in understanding the underlying conditions leading to mental retardation will undoubtedly be gained from a closer collaboration of geneticists, physiologists and cognitive neuroscientists, which should enable the establishment of standardized approaches.