bluuebunny/crossref_metadata_2025_split huggingface dataset:
World Health Organization 2006 Child Growth Standards and 2007 Growth Reference Charts
Authors: Turck Dominique , Michaelsen Kim F. , Shamir Raanan , Braegger Christian , Campoy Cristina , Colomb Virginie , Decsi Tamás , Domellöf Magnus , Fewtrell Mary , Kolacek Sanja , Mihatsch Walter , Moreno Luis A. , van Goudoever Johannes 
Published: May 2013

ABSTRACTGrowth charts are essential for evaluating children's health including their nutrition; however, the evaluation of child growth trajectories and consequently the decision to intervene are highly dependent on the growth charts used. The aim of this discussion paper of the European Society for Paediatric Gastroenterology, Hepatology, and Nutrition Committee on Nutrition is to provide information on the background and rationale of the World Health Organization (WHO) 2006 child growth standards and WHO 2007 growth reference charts, describe their development, outline their main innovative aspects, discuss potential limitations, and make recommendations. WHO 2006 child growth standards (0–5 years) are based on prospectively collected data describing the growth of healthy infants who were breast‐fed according to WHO recommendations, showing a pattern of linear growth, which is remarkably consistent between different countries and ethnic groups. WHO 2007 growth reference charts (5–19 years) are based mainly on a re‐analysis of National Centre for Health Statistics data from 1977, without information on feeding. European Society for Paediatric Gastroenterology, Hepatology, and Nutrition Committee on Nutrition recommends that WHO child growth standards should be used to monitor growth in all children in the age range 0 to 2 years in Europe, whether breast‐ or formula‐fed, and that they should be considered to be used in the age range 2 to 5 years. Implementation of the WHO child growth standards should be preceded by evaluation of the implication of their use on national healthcare policies. Health professionals should be guided on their use and interpretation and an adequate communication strategy should be available locally to ensure that parents receive clear and consistent advice. The decision on whether to implement the WHO growth references (5–19 years) should be made by national bodies because the growth pattern during the 5‐ to 19‐year period differs between populations.
Endoscopic and Histologic Analysis of Gastric Mucosa‐Associated Lymphoid Tissue in Children With Helicobacter pylori Infection
Authors: Yang Hye Ran , Choi Hyoung Soo , Paik Jin Ho , Lee Hye Seung 
Published: May 2013

ABSTRACTObjectives:Nodular gastritis (NG) associated with Helicobacter pylori infection can occur commonly in childhood and is regarded to be benign without clinical significance. This study includes endoscopic and histologic analysis of gastric mucosa‐associated lymphoid tissue (MALT) to clarify the significance of NG on endoscopy in H pylori–infected children.Methods:Of the 758 children who underwent endoscopy, 80 were identified as having H pylori infection. These patients were divided into 3 groups based on endoscopic severity of gastric nodularity. Histopathologic grading of MALT and immunohistochemistry of CD3, CD20, cytokeratin, and Ki‐67 were evaluated.Results:On endoscopy, severe NG was observed in the antrum of 38 of the 80 subjects, mild NG in 27, and an absence of NG in 15. Density of H pylori and lymphocyte infiltration differed among the 3 groups (P = 0.022 and P = 0.025, respectively). Histological grading for gastric lymphoid infiltrates was compatible with grade 1 in 47 (58.8%), grade 2 in 21 (26.3%), grade 3 in 7 (8.8%), and grade 4–5 in 4 (5.1%) in the antrum. Degree of NG, density of H pylori, neutrophil activity, and gastritis score in the antrum varied with MALT grades (P = 0.003, P = 0.042, P = 0.028, and P = 0.006, respectively).Conclusions:Our study suggests NG may present as a significant gastric manifestation of childhood H pylori infection that indicates gastric MALT. Thorough histologic investigation may be useful in the evaluation of gastric MALT in children infected with H pylori that manifests as severe NG in the antrum.
Negative Feedback Control of Jasmonate Signaling by an Alternative Splice Variant of JAZ10
Authors: Moreno Javier E. , Shyu Christine , Campos Marcelo L. , Patel Lalita C. , Chung Hoo Sun , Yao Jian , He Sheng Yang , Howe Gregg A. 
Published: May 2013

Abstract
The plant hormone jasmonate (JA) activates gene expression by promoting ubiquitin-dependent degradation of jasmonate ZIM domain (JAZ) transcriptional repressor proteins. A key feature of all JAZ proteins is the highly conserved Jas motif, which mediates both JAZ degradation and JAZ binding to the transcription factor MYC2. Rapid expression of JAZ genes in response to JA is thought to attenuate JA responses, but little is known about the mechanisms by which newly synthesized JAZ proteins exert repression in the presence of the hormone. Here, we show in Arabidopsis (Arabidopsis thaliana) that desensitization to JA is mediated by an alternative splice variant (JAZ10.4) of JAZ10 that lacks the Jas motif. Unbiased protein-protein interaction screens identified three related basic helix-loop-helix transcription factors (MYC2, MYC3, and MYC4) and the corepressor NINJA as JAZ10.4-binding partners. We show that the amino-terminal region of JAZ10.4 contains a cryptic MYC2-binding site that resembles the Jas motif and that the ZIM motif of JAZ10.4 functions as a transferable repressor domain whose activity is associated with the recruitment of NINJA. Functional studies showed that the expression of JAZ10.4 from the native JAZ10 promoter complemented the JA-hypersensitive phenotype of a jaz10 mutant. Moreover, treatment of these complemented lines with JA resulted in the rapid accumulation of JAZ10.4 protein. Our results provide an explanation for how the unique domain architecture of JAZ10.4 links transcription factors to a corepressor complex and suggest how JA-induced transcription and alternative splicing of JAZ10 premessenger RNA creates a regulatory circuit to attenuate JA responses.
A Chloroplast ABC1-like Kinase Regulates Vitamin E Metabolism in Arabidopsis
Authors: Martinis Jacopo , Glauser Gaétan , Valimareanu Sergiu , Kessler Felix 
Published: May 2013

Abstract
In bacteria and mitochondria, ABC1 (for Activity of bc1 complex)-like kinases regulate ubiquinone synthesis, mutations causing severe respiration defects, including neurological disorders in humans. Little is known about plant ABC1-like kinases; in Arabidopsis (Arabidopsis thaliana), five are predicted in mitochondria but, surprisingly, six are located at lipid droplets in chloroplasts. These are a known site of prenylquinone (including tocopherol [vitamin E], phylloquinone [vitamin K] and plastoquinone) metabolism and contain a large proportion of the tocopherol cyclase (VTE1) required for vitamin E synthesis and recycling. Therefore, ABC1-like kinases may be involved in the regulation of chloroplast prenylquinone metabolism. Using a nontargeted lipidomics approach, we demonstrate that plants lacking the plastoglobule ABC1-like kinase ABC1K3 are defective both for the production of plastochromanol-8 (a plastoquinone-derived lipid antioxidant) and the redox recycling of α-tocopherol, whereas tocopherol production is not affected. All of these pathways require VTE1 activity. However, in the abc1k3 mutant, VTE1 levels are strongly reduced posttranscriptionally. We provide evidence that the ABC1-like kinase ABC1K3 phosphorylates VTE1, possibly stabilizing it at plastoglobules. However, ABC1K3 may also have other targets and be involved in a wider chloroplast regulatory network.
Factor Xa Inhibitor Attenuates Leukocyte Adhesion and Thrombus Formation in an Experimental Mouse Model of the Metabolic Syndrome
Authors: Iba Toshiaki , Aihara Koichiro , Watanabe Shin , Yanagawa Youichi , Yamada Atushi , Koichiro Niwa , Ohsaka Akimichi 
Published: May 2013

SummaryAimsIn a model of acute inflammation, Factor Xa inhibitors have been reported not only to suppress the coagulation system but also to exert anti‐inflammatory effects. However, this has not been experimentally demonstrated in a model of chronic inflammation. Recent studies demonstrated that vascular inflammation in the metabolic syndrome plays major roles in the development of thrombotic diseases. Therefore, we examined the anti‐inflammatory effects of fondaparinux, a Factor Xa inhibitor, in a mouse model of the metabolic syndrome, looking at both leukocyte adhesion on the vascular endothelium and thrombus formation.MethodsFollowing clamping of the mesenteric vein for 20 min in the KK‐Ay mouse, mice were administered by subcutaneous injection either low‐dose or high‐dose fondaparinux or placebo (n = 10 in each group. Microscopic observation of the intestinal microcirculation was carried out. In another series, blood samples were taken and measured for blood cell counts and organ damage markers (n = 6 in each).ResultsBoth leukocyte adherence and thrombus formation were inhibited by treatment with fondaparinux. Red blood cell and white blood cell counts were maintained better in high‐dose group. Levels of alanine aminotransferase (ALT) were significantly reduced in both low‐dose and high‐dose groups (P < 0.05 and 0.01, compared with control, respectively).ConclusionsFactor Xa inhibitor attenuates leukocyte adhesion and leukocyte‐platelet conjugate formation in a mouse model of the metabolic syndrome. These effects appeared to be related to both inhibition of thrombus formation and reduction in markers of organ damage.
Reduced α‐synuclein levels in cerebrospinal fluid in Parkinson's disease are unrelated to clinical and imaging measures of disease severity
Authors: van Dijk K. D. , Bidinosti M. , Weiss A. , Raijmakers P. , Berendse H. W. , van de Berg W. D. J. 
Published: May 2013

Background and purposeThe cerebrospinal fluid (CSF) concentration of α‐synuclein may reflect the aggregation of α‐synuclein in brain tissue that neuropathologically characterizes Parkinson's disease (PD). Although most studies in large cohorts report reduced CSF α‐synuclein levels in PD, the available data to date are not consistent due to variation in group sizes, pre‐analytical confounding factors and assay characteristics. Furthermore, it remains unclear whether CSF α‐synuclein concentrations correlate with measures of disease severity. Acknowledging the methodological issues that emerged from previous studies, we evaluated whether CSF α‐synuclein levels differ between patients with PD and controls, and relate to disease duration or severity.Methodsα‐Synuclein levels were measured in CSF samples of 53 well‐characterized patients with PD and 50 healthy controls employing a recently developed time‐resolved Förster's resonance energy transfer assay. In addition, we studied the relationship of CSF α‐synuclein levels with disease duration, clinical measures of disease severity and the striatal dopaminergic deficit as measured by dopamine transporter binding and single photon emission computed tomography.ResultsIn patients with PD, we observed a decrease in mean CSF α‐synuclein levels that was unrelated to disease duration or measures of disease severity. Using total protein normalized α‐synuclein, a sensitivity and specificity of 70% and 74% could be reached for distinguishing between patients with PD and controls.ConclusionCSF α‐synuclein levels are reduced in patients with PD compared with healthy controls. However, sensitivity and specificity indicate that α‐synuclein will not suffice as a single biomarker. CSF α‐synuclein levels do not correlate with measures of disease severity, including striatal dopaminergic deficit.
Being Penn State: The Role of Joe Paterno's Prototypicality in the Sandusky Sex-Abuse Scandal
Authors: Wiley Shaun , Dahling Jason J. 
Published: May 2013

More than any other man, Mr. Paterno is Penn State – the man who brought the institution national recognition, the man who built a football program based on honor for 46 years, the winningest football coach in Division I history…Paterno is at the core of the university's sense of identity. (Guarino, 2011, November 10)We believe that Alderfer's (2013) intergroup analysis of the Penn State scandal can be enriched by focusing on the special role that Joe Paterno played in the events leading up to the 2010 grand jury that brought the scandal to light outside the university community. On the basis of the social identity theory of leadership (Hogg, 2001), we argue that the community afforded Paterno the trust that he appears to have abused to suppress the scandal because he embodied the norms, values, and goals of Penn State in a way that made him prototypical of the university. By making the broader group category salient, Paterno was able to shape the behavior of representatives of many sub-groups described by Alderfer within the administration, athletics, and community. Coupled with a high degree of institutional ambiguity, Paterno's prototypicality likely enabled him to suppress the “constructive diversity” (p. 123) of checks and balances that should have operated at Penn State. This disruption to effective intergroup processes prohibited necessary oversight over the PSU athletic program and the Second Mile that otherwise might have uncovered Jerry Sandusky's crimes much earlier.
SIR DYNAMICS WITH ECONOMICALLY DRIVEN CONTACT RATES
Authors: MORIN BENJAMIN R. , FENICHEL ELI P. , CASTILLO‐CHAVEZ CARLOS 
Published: May 2013

AbstractThe susceptible‐infected‐recovered (SIR) model has greatly evidenced epidemiology despite its apparent simplicity. Most applications of the SIR framework use a form of nonlinear incidence to describe the number of new cases per instant. We adapt theorems to analyze the stability of SIR models with a generalized nonlinear incidence structure. These theorems are then applied to the case of standard incidence and incidence resulting from adaptive behavioral response based on epidemiological‐economic theory. When adaptive behavior is included in the SIR model multiple equilibria and oscillatory epidemiological dynamics can occur over a greater parameter space. Our analysis, based on the epidemiological‐economic incidence, provides new insights into epidemics as complex adaptive systems, highlights important nonlinearities that lead to complex behavior, and provides mechanistic motivation for a shift away from standard incidence, and outlines important areas of research related to the complex‐adaptive dynamics of epidemics.
Cell Host Response to Infection with Novel Human Coronavirus EMC Predicts Potential Antivirals and Important Differences with SARS Coronavirus
Authors: Josset Laurence , Menachery Vineet D. , Gralinski Lisa E. , Agnihothram Sudhakar , Sova Pavel , Carter Victoria S. , Yount Boyd L. , Graham Rachel L. , Baric Ralph S. , Katze Michael G. 
Published: May 2013

ABSTRACT

A novel human coronavirus (HCoV-EMC) was recently identified in the Middle East as the causative agent of a severe acute respiratory syndrome (SARS) resembling the illness caused by SARS coronavirus (SARS-CoV). Although derived from the CoV family, the two viruses are genetically distinct and do not use the same receptor. Here, we investigated whether HCoV-EMC and SARS-CoV induce similar or distinct host responses after infection of a human lung epithelial cell line. HCoV-EMC was able to replicate as efficiently as SARS-CoV in Calu-3 cells and similarly induced minimal transcriptomic changes before 12 h postinfection. Later in infection, HCoV-EMC induced a massive dysregulation of the host transcriptome, to a much greater extent than SARS-CoV. Both viruses induced a similar activation of pattern recognition receptors and the interleukin 17 (IL-17) pathway, but HCoV-EMC specifically down-regulated the expression of several genes within the antigen presentation pathway, including both type I and II major histocompatibility complex (MHC) genes. This could have an important impact on the ability of the host to mount an adaptive host response. A unique set of 207 genes was dysregulated early and permanently throughout infection with HCoV-EMC, and was used in a computational screen to predict potential antiviral compounds, including kinase inhibitors and glucocorticoids. Overall, HCoV-EMC and SARS-CoV elicit distinct host gene expression responses, which might impact
in vivo
pathogenesis and could orient therapeutic strategies against that emergent virus.

IMPORTANCE
Identification of a novel coronavirus causing fatal respiratory infection in humans raises concerns about a possible widespread outbreak of severe respiratory infection similar to the one caused by SARS-CoV. Using a human lung epithelial cell line and global transcriptomic profiling, we identified differences in the host response between HCoV-EMC and SARS-CoV. This enables rapid assessment of viral properties and the ability to anticipate possible differences in human clinical responses to HCoV-EMC and SARS-CoV. We used this information to predict potential effective drugs against HCoV-EMC, a method that could be more generally used to identify candidate therapeutics in future disease outbreaks. These data will help to generate hypotheses and make rapid advancements in characterizing this new virus.
Anthrax Toxin-Mediated Delivery of thePseudomonasExotoxin A Enzymatic Domain to the Cytosol of Tumor Cells via Cleavable Ubiquitin Fusions
Authors: Bachran Christopher , Morley Thomas , Abdelazim Suzanne , Fattah Rasem J. , Liu Shihui , Leppla Stephen H. 
Published: May 2013

ABSTRACTAnthrax toxin proteins fromBacillus anthracisconstitute a highly efficient system for delivering cytotoxic enzymes to the cytosol of tumor cells. However, exogenous proteins delivered to the cytosol of cells are subject to ubiquitination on lysines and proteasomal degradation, which limit their potency. We created fusion proteins containing modified ubiquitins with their C-terminal regions fused to thePseudomonasexotoxin A catalytic domain (PEIII) in order to achieve delivery and release of PEIII to the cytosol. Fusion proteins in which all seven lysines of wild-type ubiquitin were retained while the site cleaved by cytosolic deubiquitinating enzymes (DUBs) was removed were nontoxic, apparently due to rapid ubiquitination and proteasomal degradation. Fusion proteins in which all lysines of wild-type ubiquitin were substituted by arginine had high potency, exceeding that of a simple fusion lacking ubiquitin. This variant was less toxic to nontumor tissues in mice than the fusion protein lacking ubiquitin and was very efficient for tumor treatment in mice. The potency of these proteins was highly dependent on the number of lysines retained in the ubiquitin domain and on retention of the C-terminal ubiquitin sequence cleaved by DUBs. It appears that rapid cytosolic release of a cytotoxic enzyme (e.g., PEIII) that is itself resistant to ubiquitination is an effective strategy for enhancing the potency of tumor-targeting toxins.IMPORTANCEBacterial toxins typically have highly efficient mechanisms for cellular delivery of their enzymatic components. Cytosolic delivery of therapeutic enzymes and drugs is an important topic in molecular medicine. We describe anthrax toxin fusion proteins containing ubiquitin as a cytosolic cleavable linker that improves the delivery of an enzyme to mammalian cells. The ubiquitin linker allowed modulation of potency in cells and in mice. This effective strategy for enhancing the intracellular potency of an enzyme may be useful for the cytosolic delivery and release of internalized drugs.
Opposing Roles for Two Molecular Forms of Replication Protein A in Rad51-Rad54-Mediated DNA Recombination in Plasmodium falciparum
Authors: Gopalakrishnan Anusha M. , Kumar Nirbhay 
Published: May 2013

ABSTRACT

The bacterial RecA protein and its eukaryotic homologue Rad51 play a central role in the homologous DNA strand exchange reaction during recombination and DNA repair. Previously, our lab has shown that PfRad51, the
Plasmodium falciparum
homologue of Rad51, exhibited ATPase activity and promoted DNA strand exchange
in vitro
. In this study, we evaluated the catalytic functions of PfRad51 in the presence of putative interacting partners, especially
P. falciparum
homologues of Rad54 and replication protein A. PfRad54 accelerated PfRad51-mediated pairing between single-stranded DNA (ssDNA) and its homologous linear double-stranded DNA (dsDNA) in the presence of 0.5 mM CaCl
2
. We also present evidence that recombinant PfRPA1L protein serves the function of the bacterial homologue single-stranded binding protein (SSB) in initiating homologous pairing and strand exchange activity. More importantly, the function of PfRPA1L was negatively regulated in a dose-dependent manner by PfRPA1S, another RPA homologue in
P. falciparum
. Finally, we present
in vivo
evidence through comet assays for methyl methane sulfonate-induced DNA damage in malaria parasites and accompanying upregulation of PfRad51, PfRad54, PfRPA1L, and PfRPA1S at the level of transcript and protein needed to repair DNA damage. This study provides new insights into the role of putative Rad51-interacting proteins involved in homologous recombination and emphasizes the physiological role of DNA damage repair during the growth of parasites.

IMPORTANCE
Homologous recombination plays a major role in chromosomal rearrangement, and Rad51 protein, aided by several other proteins, plays a central role in DNA strand exchange reaction during recombination and DNA repair. This study reports on the characterization of the role of
P. falciparum
Rad51 in homologous strand exchange and DNA repair and evaluates the functional contribution of PfRad54 and PfRPA1 proteins. Data presented here provide mechanistic insights into DNA recombination and DNA damage repair mechanisms in this parasite. The importance of these research findings in future work will be to investigate if Rad51-dependent mechanisms are involved in chromosomal rearrangements during antigenic variation in
P. falciparum
. A prominent determinant of antigenic variation, the extraordinary ability of the parasite to rapidly change its surface molecules, is associated with
var
genes, and antigenic variation presents a major challenge to vaccine development.
Injury surveillance in the World Football Tournaments 1998–2012
Authors: Junge Astrid , Dvorak Jiri 
Published: May 2013

BackgroundInternational sports bodies should protect the health of their athletes, and injury surveillance is an important pre-requisite for injury prevention. The Fédération International de Football Association (FIFA) has systematically surveyed all football injuries in their tournaments since 1998.AimsAnalysis of the incidence, characteristics and changes of football injury during international top-level tournaments 1998–2012.MethodsAll newly incurred football injuries during the FIFA tournaments and the Olympic Games were reported by the team physicians on a standardised injury report form after each match. The average response rate was 92%.ResultsA total of 3944 injuries were reported from 1546 matches, equivalent to 2.6 injuries per match. The majority of injuries (80%) was caused by contact with another player, compared with 47% of contact injuries by foul play. The most frequently injured body parts were the ankle (19%), lower leg (16%) and head/neck (15%). Contusions (55%) were the most common type of injury, followed by sprains (17%) and strains (10%). On average, 1.1 injuries per match were expected to result in absence from a match or training. The incidence of time-loss injuries was highest in the FIFA World Cups and lowest in the FIFA U17 Women's World Cups. The injury rates in the various types of FIFA World Cups had different trends over the past 14 years.ConclusionsChanges in the incidence of injuries in top-level tournaments might be influenced by the playing style, refereeing, extent and intensity of match play. Strict application of the Laws of the Games is an important means of injury prevention.