bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dietary patterns and their associations with childhood obesity in China
Authors: Zhang Jiguo , Wang Huijun , Wang Youfa , Xue Hong , Wang Zhihong , Du Wenwen , Su Chang , Zhang Ji , Jiang Hongru , Zhai Fengying , Zhang Bing 
Published: May 2015

Dietary patterns represent the combined effects of foods, and illustrate efficaciously the impact of diet on health outcomes. Some findings of previous studies have limited applicability to Chinese children due to cultural factors. The presnt study was designed to identify dietary patterns and determine their relationships with obesity among Chinese children and adolescents. Data collected from 1282 children and adolescents aged 7–17 years from the 2011 China Health and Nutrition Survey (CHNS) were used. Dietary patterns were identified using factor analysis of data from three consecutive 24-h dietary recalls. Weight and height were measured following standard methods, and BMI was calculated. Three dietary patterns were identified: modern (high intakes of milk, fast foods and eggs), traditional north (high intakes of wheat, tubers and other cereals) and traditional south (high intakes of vegetables, rice and pork). After adjusting for some confounders and total energy intake, subjects in the highest quartiles of the modern and traditional north patterns were found to have significantly greater risk of obesity (OR 3·10, 95 % CI 1·52, 6·32, and OR 2·42, 95 % CI 1·34, 4·39, respectively). In conclusion, the modern dietary pattern and the traditional north dietary pattern were associated with higher risk of obesity. Promoting healthier eating patterns could help prevent obesity in Chinese children.
Canadian power mobility device users' experiences of ageing with mobility impairments
Authors: KOROTCHENKO ALEXANDRA , HURD CLARKE LAURA 
Published: May 2015

ABSTRACTIn this article, we draw upon interviews with 14 men and 15 women aged 51–92 to examine the embodied experiences of Canadian power mobility device users. In particular, we investigate how individuals ageing with mobility impairments perceived and experienced the practical impacts and symbolic cultural connotations of utilising a power mobility device. Our findings reveal that those participants who had begun to use their power mobility devices later in life were dismayed by and apprehensive about the significance of their diminishing physical abilities in the context of the societal privileging of youthful and able bodies. At the same time, the participants who had used a power mobility device from a young age were fearful of prospective bodily declines, and discussed the significance and consequences of being unable to continue to operate their power mobility devices autonomously in the future. We consider the ways in which the participants attempted to manage, mitigate and reframe their experiences of utilising power mobility devices in discriminatory environments. We discuss our findings in relation to on-going theoretical debates pertaining to the concepts of ‘biographical disruption’ and the third and fourth ages.
Prenatal tobacco exposure and self-regulation in early childhood: Implications for developmental psychopathology
Authors: Wiebe Sandra A. , Clark Caron A. C. , De Jong Desiree M. , Chevalier Nicolas , Espy Kimberly Andrews , Wakschlag Lauren 
Published: May 2015

AbstractPrenatal tobacco exposure (PTE) has a well-documented association with disruptive behavior in childhood, but the neurocognitive effects of exposure that underlie this link are not sufficiently understood. The present study was designed to address this gap, through longitudinal follow-up in early childhood of a prospectively enrolled cohort with well-characterized prenatal exposure. Three-year-old children (n= 151) were assessed using a developmentally sensitive battery capturing both cognitive and motivational aspects of self-regulation. PTE was related to motivational self-regulation, where children had to delay approach to attractive rewards, but not cognitive self-regulation, where children had to hold information in mind and inhibit prepotent motor responses. Furthermore, PTE predicted motivational self-regulation more strongly in boys than in girls, and when propensity scores were covaried to control for confounding risk factors, the effect of PTE on motivational self-regulation was significant only in boys. These findings suggest that PTE's impact on neurodevelopment may be greater in boys than in girls, perhaps reflecting vulnerability in neural circuits that subserve reward sensitivity and emotion regulation, and may also help to explain why PTE is more consistently related to disruptive behavior disorders than attention problems.
Brain adaptation and alternative developmental trajectories
Authors: Johnson Mark H. , Jones Emily J. H. , Gliga Teodora 
Published: May 2015

AbstractResilience and adaptation in the face of early genetic or environmental risk has become a major interest in child psychiatry over recent years. However, we still remain far from an understanding of how developing human brains as a whole adapt to the diffuse and widespread atypical synaptic function that may be characteristic of some common developmental disorders. The first part of this paper discusses four types of whole-brain adaptation in the face of early risk: redundancy, reorganization, niche construction, and adjustment of developmental rate. The second part of the paper applies these adaptation processes specifically to autism. We speculate that key features of autism may be the end result of processes of early brain adaptation, rather than the direct consequences of ongoing neural pathology.
Neural plasticity and the development of attention: Intrinsic and extrinsic influences
Authors: Swingler Margaret M. , Perry Nicole B. , Calkins Susan D. 
Published: May 2015

AbstractThe development of attention has been strongly linked to the regulation of emotion and behavior and has therefore been of particular interest to researchers aiming to better understand precursors to behavioral maladjustment. In the current paper, we utilize a developmental psychopathology and neural plasticity framework to highlight the importance of both intrinsic (i.e., infant neural functioning) and extrinsic (i.e., caregiver behavior) factors for the development of attentional control across the first year. We begin by highlighting the importance of attention for children's emotion regulation abilities and mental health. We then review the development of attention behavior and underscore the importance of neural development and caregiver behavior for shaping attentional control. Finally, we posit that neural activation associated with the development of the executive attention network may be one mechanism through which maternal caregiving behavior influences the development of infants’ attentional control and subsequent emotion regulation abilities known to be influential to childhood psychopathology.
Developmental psychopathology in an era of molecular genetics and neuroimaging: A developmental neurogenetics approach
Authors: Hyde Luke W. 
Published: May 2015

AbstractThe emerging field of neurogenetics seeks to model the complex pathways from gene to brain to behavior. This field has focused on imaging genetics techniques that examine how variability in common genetic polymorphisms predict differences in brain structure and function. These studies are informed by other complimentary techniques (e.g., animal models and multimodal imaging) and have recently begun to incorporate the environment through examination of Imaging Gene × Environment interactions. Though neurogenetics has the potential to inform our understanding of the development of psychopathology, there has been little integration between principles of neurogenetics and developmental psychopathology. The paper describes a neurogenetics and Imaging Gene × Environment approach and how these approaches have been usefully applied to the study of psychopathology. Six tenets of developmental psychopathology (the structure of phenotypes, the importance of exploring mechanisms, the conditional nature of risk, the complexity of multilevel pathways, the role of development, and the importance of who is studied) are identified, and how these principles can further neurogenetics applications to understanding the development of psychopathology is discussed. A major issue of this piece is how neurogenetics and current imaging and molecular genetics approaches can be incorporated into developmental psychopathology perspectives with a goal of providing models for better understanding pathways from among genes, environments, the brain, and behavior.
Dysplasticity, metaplasticity, and schizophrenia: Implications for risk, illness, and novel interventions
Authors: Keshavan Matcheri S. , Mehta Urvakhsh Meherwan , Padmanabhan Jaya L. , Shah Jai L. 
Published: May 2015

AbstractIn this paper, we review the history of the concept of neuroplasticity as it relates to the understanding of neuropsychiatric disorders, using schizophrenia as a case in point. We briefly review the myriad meanings of the term neuroplasticity, and its neuroscientific basis. We then review the evidence for aberrant neuroplasticity and metaplasticity associated with schizophrenia as well as the risk for developing this illness, and discuss the implications of such understanding for prevention and therapeutic interventions. We argue that the failure and/or altered timing of plasticity of critical brain circuits might underlie cognitive and deficit symptoms, and may also lead to aberrant plastic reorganization in other circuits, leading to affective dysregulation and eventually psychosis. This “dysplastic” model of schizophrenia can suggest testable etiology and treatment-relevant questions for the future.
Structural aspects of dormancy in quinoa (Chenopodium quinoa): importance and possible action mechanisms of the seed coat
Authors: Ceccato Diana , Bertero Daniel , Batlla Diego , Galati Beatriz 
Published: May 2015

AbstractTwo possible sources of resistance to pre-harvest sprouting were evaluated in quinoa. They showed dormancy at harvest and significant variations in dormancy level in response to environmental conditions experienced during seed development. The aims of this work were to evaluate the importance of seed coats in the regulation of dormancy in this species, to investigate possible mechanisms of action and to assess association of seed coat properties with changes in dormancy level caused by the environment. Accessions Chadmo and 2-Want were grown under field conditions on different sowing dates during 2 years. Seed coats were manipulated and seed germination was evaluated at different temperatures. Seed coat perforation before incubation led to faster dormancy loss in both accessions. This effect decreased with delayed sowing date, and seeds expressed a level of dormancy not imposed by coats. This suggests the presence of embryo dormancy in the genus Chenopodium. Seeds of the accession 2-Want had a significantly thinner seed coat at later sowing dates, associated with a decreasing coat-imposed dormancy, but this pattern was not detected in Chadmo. The seed coat acts as a barrier to the release of endogenous abscisic acid (ABA) in quinoa, suggested by the increase in germination and a higher amount of ABA leached from perforated seeds. ABA is able to leach from seeds with an intact seed coat, suggesting that differences in seed coat thickness may allow the leakage of different amounts of ABA. This mechanism may contribute to the observed differences in dormancy level, either between sowing dates or between accessions.
Acetylation of HDAC1 and degradation of SIRT1 form a positive feedback loop to regulate p53 acetylation during heat-shock stress
Authors: Yang H , Yan B , Liao D , Huang S , Qiu Y 
Published: May 2015

AbstractThe tumor suppressor p53 is an essential transcription factor that sensitively regulates cellular responses to various stresses. Acetylation, a critically important posttranslational modification of p53, is induced in response to cellular stresses. P53 acetylation level strongly correlates with protein stability and activity. The steady-state level of p53 acetylation is balanced by dynamic acetylation and deacetylation. Despite the function of p53 acetylation being well studied, how the steady state of p53 acetylation level is regulated in response to cellular stresses remains unclear. In particular, the dynamic regulation of the deacetylase activities responsible for p53 deacetylation during cellular stress is unknown. In the current study, we investigated the dynamic regulation of HDAC1 (histone deacetylase 1) and SIRT1 (sirtuin 1), two major enzymes for p53 deacetylation, during cell stress. We found that various cell stress events induce HDAC1 acetylation. The increased level of HDAC1 acetylation correlates with the level of p53 acetylation. Acetylated HDAC1 loses the ability to deacetylate p53. Cellular stresses also promote the decline of the SIRT1 protein in a proteasome-dependent pathway, which also results in the increase of p53 acetylation. Importantly, the decreased level of SIRT1 also contributes to the accumulation of HDAC1 acetylation as SIRT1 deacetylates HDAC1. Therefore, the increase of HDAC1 acetylation and reduced level of SIRT1 protein during cellular stress directly link to the induction of p53 acetylation. These results unveil the mechanism underlying the dynamic regulation of p53 acetylation during cell stress.
ErbB2-intronic MicroRNA-4728: a novel tumor suppressor and antagonist of oncogenic MAPK signaling
Authors: Schmitt D C , Madeira da Silva L , Zhang W , Liu Z , Arora R , Lim S , Schuler A M , McClellan S , Andrews J F , Kahn A G , Zhou M , Ahn E-YE , Tan M 
Published: May 2015

AbstractAlthough the role of the ErbB2/HER2 oncogene in cancers has been extensively studied, how ErbB2 is regulated remains poorly understood. A novel microRNA, mir-4728, was recently found within an intron of the ErbB2 gene. However, the function and clinical relevance of this intronic miRNA are completely unknown. Here, we demonstrate that mir-4728 is a negative regulator of MAPK signaling through directly targeting the ERK upstream kinase MST4 and exerts numerous tumor-suppressive properties in vitro and in animal models. Importantly, our patient sample study shows that mir-4728 was under-expressed in breast tumors compared with normal tissue, and loss of mir-4728 correlated with worse overall patient survival. These results strongly suggest that mir-4728 is a tumor-suppressive miRNA that controls MAPK signaling through targeting MST4, revealing mir-4728’s significance as a potential prognostic factor and target for therapeutic intervention in cancer. Moreover, this study represents a conceptual advance by providing strong evidence that a tumor-suppressive miRNA can antagonize the canonical signaling of its host oncogene.
The synergistic interaction between the calcineurin B subunit and IFN-γ enhances macrophage antitumor activity
Authors: Su Z , Yang R , Zhang W , Xu L , Zhong Y , Yin Y , Cen J , DeWitt J P , Wei Q 
Published: May 2015

AbstractMacrophages are involved in tumor growth and progression. They infiltrate into tumors and cause inflammation, which creates a microenvironment favoring tumor growth and metastasis. However, certain stimuli may induce macrophages to act as tumor terminators. Here we report that the calcineurin B subunit (CnB) synergizes with IFN-γ to make macrophages highly cytotoxic to cancer cells. Furthermore, CnB and IFN-γ act synergistically to polarize mouse tumor-associated macrophages, as well as human monocyte-derived macrophages to an M1-like phenotype. This synergy is mediated by the crosstalk between CnB-engaged integrin αM-p38 MAPK signaling and IFN-γ-initiated p38/PKC-δ/Jak2 signaling. Interestingly, the signal transducer and activator of transcription 1 (STAT1) is a key factor that orchestrates the synergy of CnB and IFN-γ, and the phosphorylation status at Ser727 and Tyr701 of STAT1 is directly regulated by CnB and IFN-γ.
Prdx4 is a compartment-specific H2O2 sensor that regulates neurogenesis by controlling surface expression of GDE2
Authors: Yan Ye , Wladyka Cynthia , Fujii Junichi , Sockanathan Shanthini 
Published: May 2015

AbstractNeural progenitors and terminally differentiated neurons show distinct redox profiles, suggesting that coupled-redox cascades regulate the initiation and progression of neuronal differentiation. Discrete cellular compartments have different redox environments and how they contribute to differentiation is unclear. Here we show that Prdx4, an endoplasmic reticulum (ER) enzyme that metabolizes H2O2, acts as a tunable regulator of neurogenesis via its compartmentalized thiol-oxidative function. Prdx4 ablation causes premature motor neuron differentiation and progenitor depletion, leading to imbalances in subtype-specific motor neurons. GDE2, a six-transmembrane protein that induces differentiation by downregulating Notch signalling through surface cleavage of GPI-anchored proteins, is targeted by Prdx4 oxidative activity. Prdx4 dimers generated by H2O2 metabolism oxidize two cysteine residues within the GDE2 enzymatic domain, which blocks GDE2 trafficking to the plasma membrane and prevents GDE2 neurogeneic function. Thus, Prdx4 oxidative activity acts as a sensor to directly couple neuronal differentiation with redox environments in the ER.
Extreme 13C depletion of carbonates formed during oxidation of biogenic methane in fractured granite
Authors: Drake Henrik , Åström Mats E. , Heim Christine , Broman Curt , Åström Jan , Whitehouse Martin , Ivarsson Magnus , Siljeström Sandra , Sjövall Peter 
Published: May 2015

AbstractPrecipitation of exceptionally 13C-depleted authigenic carbonate is a result of, and thus a tracer for, sulphate-dependent anaerobic methane oxidation, particularly in marine sediments. Although these carbonates typically are less depleted in 13C than in the source methane, because of incorporation of C also from other sources, they are far more depleted in 13C (δ13C as light as −69‰ V-PDB) than in carbonates formed where no methane is involved. Here we show that oxidation of biogenic methane in carbon-poor deep groundwater in fractured granitoid rocks has resulted in fracture-wall precipitation of the most extremely 13C-depleted carbonates ever reported, δ13C down to −125‰ V-PDB. A microbial consortium of sulphate reducers and methane oxidizers has been involved, as revealed by biomarker signatures in the carbonates and S-isotope compositions of co-genetic sulphide. Methane formed at shallow depths has been oxidized at several hundred metres depth at the transition to a deep-seated sulphate-rich saline water. This process is so far an unrecognized terrestrial sink of methane.
Expression of heterologous sigma factors enables functional screening of metagenomic and heterologous genomic libraries
Authors: Gaida Stefan M. , Sandoval Nicholas R. , Nicolaou Sergios A. , Chen Yili , Venkataramanan Keerthi P. , Papoutsakis Eleftherios T. 
Published: May 2015

AbstractA key limitation in using heterologous genomic or metagenomic libraries in functional genomics and genome engineering is the low expression of heterologous genes in screening hosts, such as Escherichia coli. To overcome this limitation, here we generate E. coli strains capable of recognizing heterologous promoters by expressing heterologous sigma factors. Among seven sigma factors tested, RpoD from Lactobacillus plantarum (Lpl) appears to be able of initiating transcription from all sources of DNA. Using the promoter GFP-trap concept, we successfully screen several heterologous and metagenomic DNA libraries, thus enlarging the genomic space that can be functionally sampled in E. coli. For an application, we show that screening fosmid-based Lpl genomic libraries in an E. coli strain with a chromosomally integrated Lpl rpoD enables the identification of Lpl genetic determinants imparting strong ethanol tolerance in E. coli. Transcriptome analysis confirms increased expression of heterologous genes in the engineered strain.
Four patients with a history of acute exacerbations of COPD: implementing the CHEST/Canadian Thoracic Society guidelines for preventing exacerbations
Authors: Tsiligianni Ioanna , Goodridge Donna , Marciniuk Darcy , Hull Sally , Bourbeau Jean 
Published: May 2015

AbstractThe American College of Chest Physicians and Canadian Thoracic Society have jointly produced evidence-based guidelines for the prevention of exacerbations in chronic obstructive pulmonary disease (COPD). This educational article gives four perspectives on how these guidelines apply to the practical management of people with COPD. A current smoker with frequent exacerbations will benefit from support to quit, and from optimisation of his inhaled treatment. For a man with very severe COPD and multiple co-morbidities living in a remote community, tele-health care may enable provision of multidisciplinary care. A woman who is admitted for the third time in a year needs a structured assessment of her care with a view to stepping up pharmacological and non-pharmacological treatment as required. The overlap between asthma and COPD challenges both diagnostic and management strategies for a lady smoker with a history of asthma since childhood. Common threads in all these cases are the importance of advising on smoking cessation, offering (and encouraging people to attend) pulmonary rehabilitation, and the importance of self-management, including an action plan supported by multidisciplinary teams.
Reduced erythrocyte susceptibility and increased host clearance of young parasites slows Plasmodium growth in a murine model of severe malaria
Authors: Khoury David S. , Cromer Deborah , Best Shannon E. , James Kylie R. , Sebina Ismail , Haque Ashraful , Davenport Miles P. 
Published: May 2015

AbstractThe best correlate of malaria severity in human Plasmodium falciparum (Pf) infection is the total parasite load. Pf-infected humans could control parasite loads by two mechanisms, either decreasing parasite multiplication, or increasing parasite clearance. However, few studies have directly measured these two mechanisms in vivo. Here, we have directly quantified host clearance of parasites during Plasmodium infection in mice. We transferred labelled red blood cells (RBCs) from Plasmodium infected donors into uninfected and infected recipients and tracked the fate of donor parasites by frequent blood sampling. We then applied age-based mathematical models to characterise parasite clearance in the recipient mice. Our analyses revealed an increased clearance of parasites in infected animals, particularly parasites of a younger developmental stage. However, the major decrease in parasite multiplication in infected mice was not mediated by increased clearance alone, but was accompanied by a significant reduction in the susceptibility of RBCs to parasitisation.