bluuebunny/crossref_metadata_2025_split huggingface dataset:
Losing ground: past history and future fate of Arctic small mammals in a changing climate
Authors: Prost Stefan , Guralnick Robert P. , Waltari Eric , Fedorov Vadim B. , Kuzmina Elena , Smirnov Nickolay , van Kolfschoten Thijs , Hofreiter Michael , Vrieling Klaas 
Published: January 2013

AbstractAccording to the IPCC, the global average temperature is likely to increase by 1.4–5.8 °C over the period from 1990 to 2100. In Polar regions, the magnitude of such climatic changes is even larger than in temperate and tropical biomes. This amplified response is particularly worrisome given that the so‐far moderate warming is already impacting Arctic ecosystems. Predicting species responses to rapid warming in the near future can be informed by investigating past responses, as, like the rest of the planet, the Arctic experienced recurrent cycles of temperature increase and decrease (glacial–interglacial changes) in the past. In this study, we compare the response of two important prey species of the Arctic ecosystem, the collared lemming and the narrow‐skulled vole, to Late Quaternary climate change. Using ancient DNA and Ecological Niche Modeling (ENM), we show that the two species, which occupy similar, but not identical ecological niches, show markedly different responses to climatic and environmental changes within broadly similar habitats. We empirically demonstrate, utilizing coalescent model‐testing approaches, that collared lemming populations decreased substantially after the Last Glacial Maximum; a result consistent with distributional loss over the same period based on ENM results. Given this strong association, we projected the current niche onto future climate conditions based on IPCC 4.0 scenarios, and forecast accelerating loss of habitat along southern range boundaries with likely associated demographic consequences. Narrow‐skulled vole distribution and demography, by contrast, was only moderately impacted by past climatic changes, but predicted future changes may begin to affect their current western range boundaries. Our work, founded on multiple lines of evidence suggests a future of rapidly geographically shifting Arctic small mammal prey communities, some of whom are on the edge of existence, and whose fate may have ramifications for the whole Arctic food web and ecosystem.
Burden of treatment for chronic illness: a concept analysis and review of the literature
Authors: Sav Adem , King Michelle A. , Whitty Jennifer A. , Kendall Elizabeth , McMillan Sara S. , Kelly Fiona , Hunter Beth , Wheeler Amanda J. 
Published: January 2013

AbstractContextTreatment burden, the burden associated with the treatment and management of chronic illness, has not yet been well articulated.ObjectiveUsing Rodgers' (1989, Journal of Advanced Nursing, 14, 330–335) method of concept analysis, this review describes the ways in which treatment burden has been conceptualized to define the concept and to develop a framework for understanding its attributes, antecedents and consequences.MethodsLeading databases were searched electronically between the years 2002 and 2011. To ensure the review focused on actual observations of the concept of interest, articles that did not measure treatment burden (either qualitatively or quantitatively) were excluded. An inductive approach was used to identify themes related to the concept of treatment burden.Main resultsThirty articles, identified from 1557 abstracts, were included in the review. The attributes of treatment burden include burden as a dynamic process, as a multidimensional concept, and comprising of both subjective and objective elements. Prominent predisposing factors (antecedents) include the person's age and gender, their family circumstances, possible comorbidity, high use of medications, characteristics of treatment and their relationship with their health‐care provider. The most dominant consequences are poor health and well‐being, non‐adherence to treatment, ineffective resource use and burden on significant others. Furthermore, many of these consequences can also become antecedents, reflecting the cyclic and dynamic nature of treatment burden.ConclusionThe findings underscore the need for researchers and health‐care professionals to engage in collaborative discussions and make cooperative efforts to help alleviate treatment burden and tailor treatment regimens to the realities of people's daily lives.
Does the calcification of adamantinomatous craniopharyngioma resemble the calcium deposition of osteogenesis/odontogenesis?
Authors: Song‐tao Qi , Xiao‐rong Yan , Jun Pan , Yong‐jian Deng , Jin Liang , Guang‐long Huang , Yun‐tao Lu , Jian Ruan , Xiang‐zhao Li , Jia‐ming Xu 
Published: January 2013

AimsCalcification in adamantinomatous craniopharyngioma (ACP) is troublesome for surgical intervention. The aim of this study was to examine the osteogenic proteins that play important roles in the calcium deposition of the odontogenic/osteogenic tissues in craniopharyngioma.Methods and resultsCraniopharyngiomas (n = 89) were investigated for the presence and expression pattern of the osteoinductive/odontoinductive factor bone morphogenetic protein‐2 (Bmp2) and two osteoblastic differentiation makers, Runt‐related transcription factor‐2 (Runx2) and Osterix, using immunohistochemistry and Western blotting. Our results showed that Bmp2, Runx2 and Osterix levels increased in cases with high calcification and correlated positively with the degree of calcification in ACP, whereas they showed little or no expression in squamous papillary craniopharyngioma. In ACP, Bmp2 was expressed primarily in the stellate reticulum and whorl‐like array cells; Runx2 and Osterix tended to be expressed in calcification‐related epithelia, including whorl‐like array cells and epithelia in/around wet keratin and calcification lesions.ConclusionsOur study indicated, for the first time, that osteogenic factor Bmp2 may play an important role in the calcification of ACP via autocrine or paracrine mechanisms. Given the presence of osteogenic markers (Runx2 and Osterix), craniopharyngioma cells could differentiate into an osteoblast‐like lineage, and the process of craniopharyngioma calcification resembles that which occurs in osteogenesis/odontogenesis.
Treatment of post‐traumatic stress disorder in patients with severe mental illness: A review
Authors: Mabey Linda , van Servellen Gwen 
Published: January 2013

AbstractAlthough the prevalence of post‐traumatic stress disorder (PTSD) is high among those with severe mental illness, little is known about the use of interventions to lessen the burden of PTSD in this population. Currently, there are limited data about safe and effective interventions to treat these individuals. This systematic published work review presents the scientific published work reporting studies of psychological treatment approaches for individuals with comorbid PTSD and severe mental illness. A secondary aim of this study was to identify the specific models implemented and tested, and their impact upon patient outcomes. A review of the published work from January 2001 through January 2012 of English‐language publications retrieved from the Cumulative Index of Nursing and Allied Health Literature (CINAHL), MEDLINE, and the American Psychological Association generated abstracts (PsycINFO) databases was conducted. Six studies met the inclusion criteria for the review. The treatment programs described were cognitive–behavioural therapy, psychoeducation, exposure‐based cognitive–behavioural therapy, and eye movement desensitization and reprocessing. Evidence of the effectiveness of these programs is examined. Data to support the use of these interventions are limited, indicating the need for further research and efficacy trials. Future areas of research and implications for nursing are discussed.
Genomics and Autism Spectrum Disorder
Authors: Johnson Norah L. , Giarelli Ellen , Lewis Celine , Rice Catherine E. 
Published: January 2013

AbstractPurpose: To present the current state of the evidence regarding translation of genetics (the study of single genes) and genomics (the study of all genes and gene‐gene or gene‐environment interactions) into health care of children with autism spectrum disorder (ASD).Methods: This article presents an overview of ASD as an international health challenge, the emerging science related to broad diagnostic criteria, and the role of the nurse in research, education, and practice.Findings: Much progress is being made in the understanding of genetics and genomics of ASD. Environmental factors are thought to contribute to the risk of developing ASD by interacting with a number of genes in different ways, thus suggesting causal heterogeneity. The rising identified prevalence of ASD, the changing diagnostic criteria for ASD, and the complexity of the core and associated features have made it difficult to define the ASD phenotype (observable behaviors that result from gene‐environment interaction). Because early identification improves opportunities for intervention, researchers are looking for a useful biomarker to detect ASD. This search is complicated by the likelihood that there are multiple causes for multiple expressions that are defined as the autism spectrum.Conclusions: To date, genetic and genomic research on ASD have underscored the complexity of the causes of ASD indicating that there are very complex genetic processes involved that are still not well understood.Clinical Relevance: Nurses will benefit from new knowledge related to early identification, diagnosis, and implications for the family to promote early intervention. Families who have a child with ASD will require nursing support for advocacy for optimal health outcomes.
An Overview of the Genomics of Metabolic Syndrome
Authors: Taylor Jacquelyn Y. , Kraja Aldi T. , de las Fuentes Lisa , Stanfill Ansley Grimes , Clark Ashley , Cashion Ann 
Published: January 2013

AbstractPurpose: This article provides a brief overview of the diagnostic criteria and genomic risk factors for the components of metabolic syndrome (MetS).Organizing Constructs: Contributions of cardiovascular, obesity, and diabetes genomic risk factors to the development of MetS as reported in the literature have been reviewed.Findings: The genomic risk factors for the development of MetS are strongly linked to the genomic risk factors that make up the components of the disease. Many of the cardiovascular and renal genomic risk factors for MetS development are similar to those found in the development of hypertension and dyslipidemia. Obesity may act as a master trigger to turn on the gene expression changes necessary for the other components of the disease. Studies in the genomics of type 2 diabetes show a number of overlapping genes and polymorphisms that influence both the development of diabetes and MetS.Conclusions: Although health practitioners now have some insights into the genomics of risk factors associated with MetS, the overall understanding of MetS remains inadequate. Clinical applications based on some of the discussed genomic risk factors are being developed but are not yet available for the diagnosis and treatment of MetS.Clinical Relevance: A broad knowledge of the genomic contributions to disease processes will enable the clinician to better utilize genomics to assess and tailor management of patients.
Gut hormone activity of children born to women with and without gestational diabetes
Authors: Chandler‐Laney P. C. , Bush N. C. , Rouse D. J. , Mancuso M. S. , Gower B. A. 
Published: January 2013

Summary
What is already known about this subject
Children born to women with gestational diabetes have greater risk for obesity.
Obesity in adults and children is associated with blunted postprandial gut hormone responses.

What this study adds
Children of women with gestational diabetes have a blunted postprandial response of GLP‐1.
Children of women with gestational diabetes have high fasting PYY concentrations.
BackgroundIntrauterine exposure to gestational diabetes mellitus (GDM) increases risk for obesity. Obesity is associated with a blunted postprandial gut hormone response, which may impair satiety and thereby contribute to weight gain. The postprandial response of gut hormones among children of women with GDM has not previously been investigated.ObjectiveTo examine whether children of women with GDM have suppressed peptide‐tyrosine‐tyrosine (PYY) and glucagon‐like‐peptide‐1 (GLP‐1), and higher concentrations of ghrelin, following a meal challenge. A secondary objective was to investigate associations of these hormones with children's free‐living energy intake.MethodsChildren (n = 42) aged 5–10 years were stratified into two groups: offspring of GDM mothers (OGD) and of non‐diabetic mothers (CTRL). Body composition was measured by dual‐energy X‐ray absorptiometry, and circulating PYY, GLP‐1 and total ghrelin were measured during a liquid meal challenge. Energy intake was assessed by three 24‐h diet recalls.ResultsBetween‐groups analyses of fasting and incremental area under the curve (AUC) found no differences in ghrelin. Incremental AUC for GLP‐1 was greater among the CTRL vs. OGD (P < 0.05), and fasting PYY, but not incremental AUC, was higher among OGD vs. CTRL (P < 0.01). Associations of fasting and incremental AUC for each gut hormone with children's usual energy intake did not differ significantly by group.ConclusionsFurther research is needed to more fully examine the potential role of postprandial GLP‐1 suppression and high‐fasting PYY concentrations on the feeding behaviour and risk for obesity among children exposed to GDM in utero.
Food insecurity, food assistance and weight status in US youth: new evidence from NHANES 2007–08
Authors: Kohn M. J. , Bell J. F. , Grow H. M. G. , Chan G. 
Published: January 2013

Summary
What is already known about this subject
Most prior work suggests no consistent association between food assistance programme participation and increased risk for youth overweight.
Previous studies have not accounted for youth food insecurity status, which may modify this relationship.

What this study adds
Associations between food assistance programme participation and youth overweight are modified by food insecurity.
In a national sample, food‐secure youth, but not food‐insecure youth, participating in food assistance programmes had increased body size both by body mass index and waist circumference measures.
ObjectiveTo investigate food assistance participation as a risk factor for overweight and obesity in youth, and food insecurity as an effect modifier.MethodsThe sample included youth ages 4–17, in families ≤200% of the federal poverty line in the 2007–2008 National Health and Nutrition Examination Survey (n = 1321). Food insecurity was measured with the US Department of Agriculture survey module. Food assistance participation was assessed for Supplemental Nutrition Assistance Program, Special Supplemental Nutrition Program for Women, Infants and Children and school meals. Body size was classified by age‐ and sex‐specific body mass index (BMI) percentile, BMI z‐score and waist circumference percentile. Regression models with direct covariate adjustment and programme‐specific propensity scores, stratified by food insecurity, estimated associations between food assistance participation and body size.ResultsFood assistance participation was not associated with increased body size among food‐insecure youth in models with direct covariate adjustment or propensity scores. Compared with low‐income, food‐secure youth not participating in food assistance, BMI z‐scores were higher among participants in models with direct covariate adjustment (0.27–0.38 SD and 0.41–0.47 SD, for boys and girls, respectively). Using propensity scores, results were similar for boys, but less so for girls.ConclusionsFood assistance programme participation is associated with increased body size in food‐secure youth, but not food‐insecure youth. Using both direct covariate adjustment and a propensity score approach, self‐selection bias may explain some, but not all, of the associations. Providing healthy food assistance that improves diet quality without contributing to excessive intake remains an important public health goal.
Monoclonal antibodies selective for α‐synuclein oligomers/protofibrils recognize brain pathology in Lewy body disorders and α‐synuclein transgenic mice with the disease‐causing A30P mutation
Authors: Fagerqvist Therese , Lindström Veronica , Nordström Eva , Lord Anna , Tucker Stina M. E. , Su Xingjian , Sahlin Charlotte , Kasrayan Alex , Andersson Jessica , Welander Hedvig , Näsström Thomas , Holmquist Mats , Schell Heinrich , Kahle Philipp J. , Kalimo Hannu , Möller Christer , Gellerfors Pär , Lannfelt Lars , Bergström Joakim , Ingelsson Martin 
Published: January 2013

AbstractInclusions of intraneuronal alpha‐synuclein (α‐synuclein) can be detected in brains of patients with Parkinson's disease and dementia with Lewy bodies. The aggregation of α‐synuclein is a central feature of the disease pathogenesis. Among the different α‐synuclein species, large oligomers/protofibrils have particular neurotoxic properties and should therefore be suitable as both therapeutic and diagnostic targets. Two monoclonal antibodies, mAb38F and mAb38E2, with high affinity and strong selectivity for large α‐synuclein oligomers were generated. These antibodies, which do not bind amyloid‐beta or tau, recognize Lewy body pathology in brains from patients with Parkinson's disease and dementia with Lewy bodies and detect pathology earlier in α‐synuclein transgenic mice than linear epitope antibodies. An oligomer‐selective sandwich ELISA, based on mAb38F, was set up to analyze brain extracts of the transgenic mice. The overall levels of α‐synuclein oligomers/protofibrils were found to increase with age in these mice, although the levels displayed a large interindividual variation. Upon subcellular fractionation, higher levels of α‐synuclein oligomers/protofibrils could be detected in the endoplasmic reticulum around the age when behavioral disturbances develop. In summary, our novel oligomer‐selective α‐synuclein antibodies recognize relevant pathology and should be important tools to further explore the pathogenic mechanisms in Lewy body disorders. Moreover, they could be potential candidates both for immunotherapy and as reagents in an assay to assess a potential disease biomarker.
Calmodulin Kinase IV–dependent CREB activation is required for neuroprotection via NMDA receptor‐PSD95 disruption
Authors: Bell Karen F. S. , Bent Russell J. , Meese‐Tamuri Saira , Ali Alicia , Forder Joan P. , Aarts Michelle M. 
Published: January 2013

AbstractNMDA‐type glutamate receptors mediate both trophic and excitotoxic signalling in CNS neurons. We have previously shown that blocking NMDAR‐ post‐synaptic density‐95 (PSD95) interactions provides significant protection from excitotoxicity and in vivo ischaemia; however, the mechanism of neuroprotection is unclear. Here, we report that blocking PSD‐95 interactions with the Tat‐NR2B9c peptide enhances a Ca2 + ‐dependent protective pathway converging on cAMP Response Element binding protein (CREB) activation. We provide evidence that Tat‐NR2B9c neuroprotection from oxygen glucose deprivation and NMDA toxicity occurs in parallel with the activation of calmodulin kinase signalling and is dependent on a sustained phosphorylation of the CREB transcription factor and its activator CaMKIV. Tat‐NR2B9c‐dependent neuroprotection and CREB phosphorylation are blocked by coapplication of CaM kinase (KN93 and STO‐609) or CREB (KG‐501) inhibitors, and by siRNA knockdown of CaMKIV. These results are mirrored in vivo in a rat model of permanent focal ischaemia. Tat‐NR2B9c application significantly reduces infarct size and causes a selective and sustained elevation in CaMKIV phosphorylation; effects which are blocked by coadministration of KN93. Thus, calcium‐dependent nuclear signalling via CaMKIV and CREB is critical for neuroprotection via NMDAR‐PSD95 blockade, both in vitro and in vivo. This study highlights the importance of maintaining neuronal function following ischaemic injury. Future stroke research should target neurotrophic and pro‐survival signal pathways in the development of novel neuroprotective strategies.
Cardiovascular Genomics
Authors: Wung Shu‐Fen , Hickey Kathleen T. , Taylor Jacquelyn Y. , Gallek Matthew J. 
Published: January 2013

AbstractPurpose: This article provides an update on cardiovascular genomics using three clinically relevant exemplars, including myocardial infarction (MI) and coronary artery disease (CAD), stroke, and sudden cardiac death (SCD).Organizational Construct: Recent advances in cardiovascular genomic research, testing, and clinical implications are presented.Methods: Genomic nurse experts reviewed and summarized recent salient literature to provide updates on three selected cardiovascular genomic conditions.Findings: Research is ongoing to discover comprehensive genetic markers contributing to many common forms of cardiovascular disease (CVD), including MI and stroke. However, genomic technologies are increasingly being used clinically, particularly in patients with long QT syndrome (LQTS) or hypertrophic cardiomyopathy (HCM) who are at risk for SCD.Conclusions: Currently, there are no clinically recommended genetic tests for many common forms of CVD even though direct‐to‐consumer genetic tests are being marketed to healthcare providers and the general public. On the other hand, genetic testing for patients with certain single gene conditions, including channelopathies (e.g., LQTS) and cardiomyopathies (e.g., HCM), is recommended clinically.Clinical Relevance: Nurses play a pivotal role in cardiogenetics and are actively engaged in direct clinical care of patients and families with a wide variety of heritable conditions. It is important for nurses to understand current development of cardiovascular genomics and be prepared to translate the new genomic knowledge into practice.
Associations of Mothers' Friendship Quality with Adolescents' Friendship Quality and Emotional Adjustment
Authors: Glick Gary C. , Rose Amanda J. , Swenson Lance P. , Waller Erika M. 
Published: January 2013

Little research has examined the association of parents' friendships with adolescent's well‐being, perhaps because the association was considered too distal. However, developmental theories suggest that contexts in which parents, but not their children, are situated may be related to child development (Bronfenbrenner,,). The current work examined associations between the quality of mothers' own friendships and their adolescent children's friendship quality and emotional adjustment. Fifth‐, eighth‐, and eleventh‐graders (N = 172) whose mothers' friendships were characterized by conflict and antagonism reported having friendships that were high in negative friendship qualities as well as elevated internalizing symptoms. These associations held after controlling for mother–child relationship quality, suggesting that mothers' friendships may have a unique association with adolescents' adjustment.
Aversive Peer Experiences on Social Networking Sites: Development of the Social Networking‐Peer Experiences Questionnaire (SN‐PEQ)
Authors: Landoll Ryan R. , La Greca Annette M. , Lai Betty S. 
Published: January 2013

Cyber victimization is an important research area, yet little is known about aversive peer experiences on social networking sites (SNSs), which are used extensively by youth and host complex social exchanges. Across samples of adolescents (n = 216) and young adults (n = 214), we developed the Social Networking‐Peer Experiences Questionnaire (SN‐PEQ) and examined its psychometric properties, distinctiveness from traditional peer victimization measures, and associations with internalized distress. The SN‐PEQ demonstrated strong factorial invariance and a single‐factor structure that was distinct from other forms of peer victimization. Negative SNS experiences were associated with youths' symptoms of social anxiety and depression, even when controlling for traditional peer victimization. Findings highlight the importance of examining the effects of aversive peer experiences that occur via social media.