bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increased stroke risk among adult asthmatic patients
Authors: Chung Wei‐Sheng , Lin Cheng‐Li , Chen Yung‐Fu , Ho Feng‐Ming , Hsu Wu‐Huei , Kao Chia‐Hung 
Published: September 2014

AbstractBackgroundWe conducted a nationwide population‐based cohort study to investigate the effects of asthma on the risk of stroke development in an Asian population.Materials and methodsNewly diagnosed asthmatic patients aged ≥ 18 years were identified, and asthma‐free controls were randomly selected from the general population and frequency matched according to age, sex and index year using records obtained from the National Health Insurance Research Database between 2000 and 2010. Both cohorts were followed up until the end of 2011 to measure the incidence of stroke. The risk of stroke was analysed using Cox proportional hazard regression models, including factors such as sex, age and comorbidities.ResultsWe followed the asthmatic patients for 104 697 person‐years and followed the nonasthmatic people for 426 729 person‐years. The incidence density rate of stroke increased in all of the groups of asthmatic patients compared with that of the controls when stratified according to sex, age and comorbidities. The hazard ratio (HR) of stroke was 1·37‐fold greater for the asthmatic cohort, compared with that for the nonasthmatic cohort, after adjusting for sex, age and comorbidities. The adjusted HR of developing stroke substantially increased with older age and the increased frequency of asthmatic exacerbation and hospitalization. The patients receiving beta‐2 agonists as a treatment exhibited a significantly greater risk of stroke compared with the patients receiving only inhaled corticosteroids, after adjusting for covariates.ConclusionAsthma may be an independent risk factor for stroke, and its severity exhibits a dose response of stroke development.
Models for transition clinics
Authors: Carrizosa Jaime , An Isabelle , Appleton Richard , Camfield Peter , Von Moers Arpad 
Published: September 2014

SummaryTransition is a purposeful, planned process that addresses the medical, psychosocial, educational, and vocational needs of adolescents and young adults with chronic medical conditions, as they advance from a pediatric and family‐centered to an adult, individual focused health care provider. This article describes some of the models for transition clinics or services for epilepsy in five countries (Canada, France, Colombia, Germany, and the United Kingdom). These models include joint adult and pediatric clinics, algorithm‐driven service, and a check list system in the context of pediatric care. Evaluation of these models is limited, and it is not possible to choose an optimal program. The attitude and motivation of health care providers may be the most important elements.
Ecosystem properties of semiarid savanna grassland in West Africa and its relationship with environmental variability
Authors: Tagesson Torbern , Fensholt Rasmus , Guiro Idrissa , Rasmussen Mads Olander , Huber Silvia , Mbow Cheikh , Garcia Monica , Horion Stéphanie , Sandholt Inge , Holm‐Rasmussen Bo , Göttsche Frank M. , Ridler Marc‐Etienne , Olén Niklas , Lundegard Olsen Jørgen , Ehammer Andrea , Madsen Mathias , Olesen Folke S. , Ardö Jonas 
Published: September 2014

AbstractThe Dahra field site in Senegal, West Africa, was established in 2002 to monitor ecosystem properties of semiarid savanna grassland and their responses to climatic and environmental change. This article describes the environment and the ecosystem properties of the site using a unique set of in situ data. The studied variables include hydroclimatic variables, species composition, albedo, normalized difference vegetation index (NDVI), hyperspectral characteristics (350–1800 nm), surface reflectance anisotropy, brightness temperature, fraction of absorbed photosynthetic active radiation (FAPAR), biomass, vegetation water content, and land‐atmosphere exchanges of carbon (NEE) and energy. The Dahra field site experiences a typical Sahelian climate and is covered by coexisting trees (~3% canopy cover) and grass species, characterizing large parts of the Sahel. This makes the site suitable for investigating relationships between ecosystem properties and hydroclimatic variables for semiarid savanna ecosystems of the region. There were strong interannual, seasonal and diurnal dynamics in NEE, with high values of ~−7.5 g C m−2 day−1 during the peak of the growing season. We found neither browning nor greening NDVI trends from 2002 to 2012. Interannual variation in species composition was strongly related to rainfall distribution. NDVI and FAPAR were strongly related to species composition, especially for years dominated by the species Zornia glochidiata. This influence was not observed in interannual variation in biomass and vegetation productivity, thus challenging dryland productivity models based on remote sensing. Surface reflectance anisotropy (350–1800 nm) at the peak of the growing season varied strongly depending on wavelength and viewing angle thereby having implications for the design of remotely sensed spectral vegetation indices covering different wavelength regions. The presented time series of in situ data have great potential for dryland dynamics studies, global climate change related research and evaluation and parameterization of remote sensing products and dynamic vegetation models.
SUMO‐targeted ubiquitin ligase RNF4 plays a critical role in preventing chromosome loss
Authors: Hirota Kouji , Tsuda Masataka , Murai Junko , Takagi Tokiyo , Keka Islam Shamima , Narita Takeo , Fujita Mari , Sasanuma Hiroyuki , Kobayashi Junya , Takeda Shunichi 
Published: September 2014

RING finger protein 4 (RNF4) represents a subclass of ubiquitin ligases that target proteins modified by the small ubiquitin‐like modifier (SUMO) for ubiquitin‐mediated degradation. We disrupted the RNF4 gene in chicken DT40 cells and found that the resulting RNF4−/− cells gradually lost proliferation capability. Strikingly, this compromised proliferation was associated with an unprecedented cellular effect: the gradual decrease in the number of intact chromosomes. In the 6 weeks after gene targeting, there was a 25% reduction in the DNA content of the RNF4−/− cells. Regarding trisomic chromosome 2, 60% of the RNF4−/− cells lost one homologue, suggesting that DNA loss was mediated by whole chromosome loss. To determine the cause of this chromosome loss, we examined cell‐cycle checkpoint pathways. RNF4−/− cells showed a partial defect in the spindle assembly checkpoint, premature dissociation of sister chromatids, and a marked increase in the number of lagging chromosomes at anaphase. Thus, combined defects in SAC and sister chromatid cohesion may result in increased lagging chromosomes, leading to chromosome loss without accompanying chromosome gain in RNF4−/− cells. We therefore propose that RNF4 plays a novel role in preventing the loss of intact chromosomes and ensures the maintenance of chromosome integrity.
Reciprocal Relations Between Emotional Self‐Efficacy Beliefs and Ego‐Resiliency Across Time
Authors: Milioni Michela , Alessandri Guido , Eisenberg Nancy , Castellani Valeria , Zuffianò Antonio , Vecchione Michele , Caprara Gian Vittorio 
Published: September 2014

AbstractThe present study examined the longitudinal relations of adolescents' self‐reported ego‐resiliency to their emotional self‐efficacy beliefs in expressing positive emotions and in managing negative emotions as they moved into early adulthood. Participants were 239 females and 211 males with a mean age of 17 years (SD = .80) at T1, 19 years (SD = .80) at T2, 21 years (SD = .82) at T3, and 25 years (SD = .80) at T4. A four‐wave cross‐lagged regression model and mediational analyses were used. In a panel structural equation model controlling for the stability of the constructs, reciprocal relationships across time were found between ego‐resiliency and emotional self‐efficacy beliefs related to the expression of positive emotions and to the management of negative emotions. Moreover, the relation between ego‐resiliency assessed at T1 and T3, and ego‐resiliency assessed at T2 and T4, was mediated through emotional self‐efficacy beliefs (at T2 and T3, respectively), and vice versa. The posited conceptual model accounted for a significant portion of variance in ego‐resiliency and has implications for understanding the development of ego‐resiliency.
Semiautomatic Extraction of Road Horizontal Alignment from a Mobile LiDAR System
Authors: Holgado‐Barco Alberto , González‐Aguilera Diego , Arias‐Sanchez Pedro , Martinez‐Sanchez Joaquin 
Published: September 2014

AbstractThis article proposes a method to semiautomatically extract the road axis through a mobile LiDAR system, a recent popular technology for transportation‐related applications, road estimation and even to enhance driver safety. In particular, the approach developed has two components: (1) the feature extraction from LiDAR data to model the road axis, and (2) the estimation of the horizontal alignment that meets the requirements and practice for a transportation authority. Given the massive and complex character of the data captured by the system, a hierarchical (coarse‐to‐fine) and robust strategy based on segmentation, parameterization and filtering, which determine the road centerline together with the geometric elements that compose its horizontal alignment, such as straight lines, circular arcs, and clothoids, has been developed and implemented. Test results using a simulated and a real data are discussed and validated. The experimental results obtained with real cases guarantying relative accuracies under 2%, being a useful approach to produce accurate estimations of the horizontal geometric features of the road alignment.
Relationships and genetic consequences of contrasting modes of speciation among endemic species of Robinsonia (Asteraceae, Senecioneae) of the Juan Fernández Archipelago, Chile, based on AFLPs and SSRs
Authors: Takayama Koji , López‐Sepúlveda Patricio , Greimler Josef , Crawford Daniel J. , Peñailillo Patricio , Baeza Marcelo , Ruiz Eduardo , Kohl Gudrun , Tremetsberger Karin , Gatica Alejandro , Letelier Luis , Novoa Patricio , Novak Johannes , Stuessy Tod F. 
Published: September 2014

Summary

This study analyses and compares the genetic signatures of anagenetic and cladogenetic speciation in six species of the genus Robinsonia (Asteraceae, Senecioneae), endemic to the Juan Fernández Islands, Chile.

Population genetic structure was analyzed by amplified fragment length polymorphism (AFLP) and microsatellite (simple sequence repeat, SSR) markers from 286 and 320 individuals, respectively, in 28 populations. Each species is genetically distinct. Previous hypotheses of classification among these species into subgenera and sections, via morphological, phytochemical, isozymic and internal transcribed spacer (ITS) data, have been confirmed, except that R. saxatilis appears to be related to R. gayana rather than R. evenia.

Analysis of phylogenetic results and biogeographic context suggests that five of these species have originated by cladogenesis and adaptive radiation on the older Robinson Crusoe Island. The sixth species, R. masafuerae, restricted to the younger Alejandro Selkirk Island, is closely related to and an anagenetic derivative of R. evenia from Robinson Crusoe.

Microsatellite and AFLP data reveal considerable genetic variation among the cladogenetically derived species of Robinsonia, but within each the genetic variation is lower, highlighting presumptive genetic isolation and rapid radiation. The anagenetically derived R. masafuerae harbors a level of genetic variation similar to that of its progenitor, R. evenia. This is the first direct comparison of the genetic consequences of anagenetic and cladogenetic speciation in plants of an oceanic archipelago.
Differential Expression of Suppressor of Cytokine Signalling Proteins in Behçet's Disease
Authors: Hamedi M. , Bergmeier L. A. , Hagi‐Pavli E. , Vartoukian S. R. , Fortune F. 
Published: September 2014

AbstractBehçet's disease (BD) is a chronic, multisystemic, recurrent vasculitis disease of unknown aetiology. Proinflammatory cytokines are a key feature of the disease, but the triggers for their induction are not well understood and/or controversial. Suppressor of cytokine signalling (SOCS) proteins which negatively regulate the JAK–STAT signalling pathway of cytokine induction may be dysregulated in BD. The expression of SOCS1 and 3 mRNA and protein was studied in peripheral blood mononuclear cells (PBMCs) and neutrophils of patients with BD and compared with healthy controls (HCs) and patients with recurrent aphthous stomatitis (RAS) using RT‐PCR, Western blot and immunohistochemistry. SOCS1 and 3 mRNA was also measured in buccal mucosal cells (BMC) of patients with BD and HCs. SOCS1 and 3 mRNA was significantly upregulated in PBMCs of patients with BD compared with HCs (P = 0.0149; P = 0.0007). In addition, there were subtle differences between expression in active and symptom‐free BD (quiescent BD). SOCS1 and SOCS 3 were also significantly upregulated in BMC from oral ulcers of BD compared with HCs (both at P = 0.0001). A differential expression of both SOCS1 and 3 was observed between PBMCs and neutrophils in patients with BD. Immunohistochemical analysis revealed differential expression of SOCS proteins in the buccal mucosa with an increased expression at the ulcer surface of ulcers than in the non‐ulcerated tissue. These observations suggest a dysregulation of the expression of these important regulators not only between patients with BD and healthy controls but also between mucosal and systemic tissues, which may reflect the nature of the aetiopathology of the disease.
Brain responses to food and weight loss
Authors: Behary Preeshila , Miras Alexander D. 
Published: September 2014

New Findings
What is the topic of this review?
This report provides an overview of how functional neuroimaging technology has accelerated our understanding of human eating behaviour.
What advances does it highlight?
The human brain responds not only to hunger and satiation, but also to the rewarding value of food. The latter is encoded in the brain reward system, which promotes the consumption of energy‐dense food and is dysregulated in the context of obesity. In the majority of obese patients, dieting‐induced weight loss is resisted by compensatory activation of the homeostatic and hedonic brain systems, whereas pharmacological and bariatric surgery interventions might be more effective in overcoming this brain response.
In this symposium report, we examine how functional neuroimaging has revolutionized the study of human eating behaviour. In the last 20 years, functional magnetic resonance and positron emission tomography techniques have enabled researchers to understand how the human brain regions that control homeostatic and hedonic eating respond to food in physiological and pathological states. Hypothalamic, brainstem, limbic and cortical brain areas form part of a well‐co‐ordinated brain system that responds to central and peripheral neuronal, hormonal and nutrient signals. Even in physiological conditions, it promotes the consumption of energy‐dense food, because this is advantageous in evolutionary terms. Its function is dysregulated in the context of obesity so as to promote weight gain and resist weight loss. Pharmacological and bariatric surgical interventions might be more successful than lifestyle interventions in inducing weight loss and maintenance because, unlike dieting, they reduce not only hunger but also the reward value of food through their actions in homeostatic and hedonic brain regions. Functional neuroimaging is a research tool that cannot be used in isolation; its findings become meaningful and useful only when combined with data from direct measures of eating behaviour. The neuroimaging technology is continuously improving and is expected to contribute further to the in‐depth understanding of the obesity phenotype and accelerate the development of more effective and safer treatments for the condition.
Essential Role of Interleukin-1 Signaling in Host Defenses Against Group B Streptococcus
Authors: Biondo Carmelo , Mancuso Giuseppe , Midiri Angelina , Signorino Giacomo , Domina Maria , Lanza Cariccio Veronica , Venza Mario , Venza Isabella , Teti Giuseppe , Beninati Concetta 
Published: September 2014

ABSTRACTSignal transduction via MyD88, an adaptor protein engaged by the Toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) family receptors, has a crucial role in host defenses against group B streptococcus (GBS). To examine the contribution of IL-1R signaling to MyD88-dependent host defenses, we analyzed GBS infection in type I IL-1R (IL-1RI)-deficient mice. Most of these animals displayed clinical signs of sepsis and neurological disease and died after a challenge with a bacterial dose that did not cause illness or death in any of the wild-type animals. Moreover, bacterial numbers in the blood and brains of the immunodefective mice were considerably increased. The ability of blood leukocytes or bone marrow-derived macrophages to kill GBSin vitrowas not affected by a lack of IL-1RI. However, it was found in a newly developed model of GBS-induced peritoneal inflammation that IL-1 signaling selectively promoted the production of the chemokines KC and MIP-1α and neutrophil recruitment. Moreover, the secretion of KC and MIP-1α, but not tumor necrosis factor alpha, by peritoneal macrophages stimulated with GBS was significantly decreased in the absence of IL-1RI. Accordingly, the number of neutrophils in the blood and the concentration of myeloperoxidase, a neutrophil marker, in infected organs were severely reduced in the immunodefective mice during GBS disease, concomitantly with a reduction in tissue KC and MIP-1α levels. In conclusion, IL-1RI plays a crucial role in host defenses against GBS by inducing the high-level production of chemokines and the subsequent recruitment of neutrophilic polymorphonuclear leukocytes to infection sites.IMPORTANCEGroup B streptococcus (GBS) is a serious and frequent human pathogen. Experimental infection with this bacterium has been widely used to understand the mechanism whereby the body’s first line of defense, represented by cells and molecules of the innate immune system, fights infections. In both humans and mice, defective function of the adaptor molecule MyD88 has been associated with extreme susceptibility to infection by GBS and other extracellular bacteria. We show here that lack of signaling by interleukin-1 (IL-1) cytokines can largely, although not completely, explain the increased susceptibility to infection observed in the absence of MyD88 function. We show, in particular, that IL-1 signaling through the IL-1 receptor promotes the production of the leukocyte attractant chemokines KC and MIP-1α and recruitment of neutrophils to GBS infection sites, thereby enabling these leukocytes to clear the infection. Our findings indicate that stimulation of IL-1 signaling may be useful as an alternative therapeutic strategy to treat GBS infections.
The Alarmin HMGN1 Contributes to Antitumor Immunity and Is a Potent Immunoadjuvant
Authors: Wei Feng , Yang De , Tewary Poonam , Li Yana , Li Sandra , Chen Xin , Howard O.M. Zack , Bustin Michael , Oppenheim Joost J. 
Published: September 2014

Abstract
Alarmins are endogenous mediators that are elicited rapidly in response to danger signals, enhancing innate and adaptive immune responses by promoting the recruitment and maturation of antigen-presenting cells (APC). The nucleosome-binding protein HMGN1 is a potent alarmin that binds TLR4 and induces antigen-specific Th1 immune responses, but its contributions to antitumor immunity have not been explored. We found that ovalbumin (OVA)-expressing EG7 mouse thymoma cells grew much faster in Hmgn1-deficient mice than littermate-matched controls. Tumor-bearing Hmgn1−/− mice generated fewer OVA-specific CD8 cells in the spleen than EG7-bearing Hmgn1+/+ mice, suggesting that HMGN1 supported T cell–mediated antitumor immunity. In addition, EG7 tumors expressing HMGN1 grew more slowly than control EG7 tumors, suggesting greater resistance to HMGN1-expressing tumors. This resistance relied on T cell–mediated immunity because it was abolished by in vivo depletion of CD4+ and CD8+ T cells. Moreover, mice vaccinated with a DNA vector expressing an HMGN1–gp100 fusion protein manifested gp100-specific, Th1-polarized immune responses, acquiring resistance to challenge with mouse B16F1 melanoma. Overall, our findings show that HMGN1 contributes to antitumor immunity and it may offer an effective adjuvant to heighten responses to cancer vaccines. Cancer Res; 74(21); 5989–98. ©2014 AACR.
Histone H1.3 Suppresses H19 Noncoding RNA Expression and Cell Growth of Ovarian Cancer Cells
Authors: Medrzycki Magdalena , Zhang Yunzhe , Zhang Weijia , Cao Kaixiang , Pan Chenyi , Lailler Nathalie , McDonald John F. , Bouhassira Eric E. , Fan Yuhong 
Published: September 2014

Abstract
Ovarian cancer is a deadly gynecologic malignancy for which novel biomarkers and therapeutic targets are imperative for improving survival. Previous studies have suggested the expression pattern of linker histone variants as potential biomarkers for ovarian cancer. To investigate the role of histone H1 in ovarian cancer cells, we characterize individual H1 variants and overexpress one of the major somatic H1 variants, H1.3, in the OVCAR-3 epithelial ovarian cancer cell line. We find that overexpression of H1.3 decreases the growth rate and colony formation of OVCAR-3 cells. We identify histone H1.3 as a specific repressor for the noncoding oncogene H19. Overexpression of H1.3 suppresses H19 expression, and knockdown of H1.3 increases its expression in multiple ovarian epithelial cancer cell lines. Furthermore, we demonstrate that histone H1.3 overexpression leads to increased occupancy of H1.3 at the H19 regulator region encompassing the imprinting control region (ICR), concomitant with increased DNA methylation and reduced occupancy of the insulator protein CTCF at the ICR. Finally, we demonstrate that H1.3 overexpression and H19 knockdown synergistically decrease the growth rate of ovarian cancer cells. Our findings suggest that H1.3 dramatically inhibits H19 expression, which contributes to the suppression of epithelial ovarian carcinogenesis. Cancer Res; 74(22); 6463–73. ©2014 AACR.
miR326 Maturation Is Crucial for VEGF-C–Driven Cortactin Expression and Esophageal Cancer Progression
Authors: Hong Chih-Chen , Chen Pai-Sheng , Chiou Jean , Chiu Ching-Feng , Yang Ching-Yao , Hsiao Michael , Chang Yi-Wen , Yu Yang-Hao , Hung Mien-Chie , Hsu Nai-Wen , Shiah Shine-Gwo , Hsu Nan-Yung , Su Jen-Liang 
Published: September 2014

Abstract
Esophageal cancer is an aggressive human malignancy with increasing incidence in the developed world. VEGF-C makes crucial contributions to esophageal cancer progression that are not well understood. Here, we report the discovery of regulatory relationship in esophageal cancers between the expression of VEGF-C and cortactin (CTTN), a regulator of the cortical actin cytoskeleton. Upregulation of CTTN expression by VEGF-C enhanced the invasive properties of esophageal squamous cell carcinoma in vitro and tumor metastasis in vivo. Mechanistic investigations showed that VEGF-C increased CTTN expression by downregulating Dicer-mediated maturation of miR326, thereby relieving the suppressive effect of miR326 on CTTN expression. Clinically, expression of Dicer and miR326 correlated with poor prognosis in patients with esophageal cancer. Our findings offer insights into how VEGF-C enhances the robust invasive and metastatic properties of esophageal cancer, which has potential implications for the development of new biomarkers or therapies in this setting. Cancer Res; 74(21); 6280–90. ©2014 AACR.