bluuebunny/crossref_metadata_2025_split huggingface dataset:
Climate warming and agricultural stressors interact to determine stream periphyton community composition
Authors: Piggott Jeremy J. , Salis Romana K. , Lear Gavin , Townsend Colin R. , Matthaei Christoph D. 
Published: June 2014

AbstractLack of knowledge about how the various drivers of global climate change will interact with multiple stressors already affecting ecosystems is the basis for great uncertainty in projections of future biological change. Despite concerns about the impacts of changes in land use, eutrophication and climate warming in running waters, the interactive effects of these stressors on stream periphyton are largely unknown. We manipulated nutrients (simulating agricultural runoff), deposited fine sediment (simulating agricultural erosion) (two levels each) and water temperature (eight levels, 0–6 °C above ambient) simultaneously in 128 streamside mesocosms. Our aim was to determine the individual and combined effects of the three stressors on the algal and bacterial constituents of the periphyton. All three stressors had pervasive individual effects, but in combination frequently produced synergisms at the population level and antagonisms at the community level. Depending on sediment and nutrient conditions, the effect of raised temperature frequently produced contrasting response patterns, with stronger or opposing effects when one or both stressors were augmented. Thus, warming tended to interact negatively with nutrients or sediment by weakening or reversing positive temperature effects or strengthening negative ones. Five classes of algal growth morphology were all affected in complex ways by raised temperature, suggesting that these measures may prove unreliable in biomonitoring programs in a warming climate. The evenness and diversity of the most abundant bacterial taxa increased with temperature at ambient but not with enriched nutrient levels, indicating that warming coupled with nutrient limitation may lead to a more evenly distributed bacterial community as temperatures rise. Freshwater management decisions that seek to avoid or mitigate the negative effects of agricultural land use on stream periphyton should be informed by knowledge of the interactive effects of multiple stressors in a warming climate.
Vulnerability of coastal ecosystems to changes in harmful algal bloom distribution in response to climate change: projections based on model analysis
Authors: Glibert Patricia M. , Icarus Allen J. , Artioli Yuri , Beusen Arthur , Bouwman Lex , Harle James , Holmes Robert , Holt Jason 
Published: June 2014

AbstractHarmful algal blooms (HABs), those proliferations of algae that can cause fish kills, contaminate seafood with toxins, form unsightly scums, or detrimentally alter ecosystem function have been increasing in frequency, magnitude, and duration worldwide. Here, using a global modeling approach, we show, for three regions of the globe, the potential effects of nutrient loading and climate change for two HAB genera, pelagic Prorocentrum and Karenia, each with differing physiological characteristics for growth. The projections (end of century, 2090–2100) are based on climate change resulting from the A1B scenario of the Intergovernmental Panel on Climate Change Institut Pierre Simon Laplace Climate Model (IPCC, IPSL‐CM4), applied in a coupled oceanographic‐biogeochemical model, combined with a suite of assumed physiological ‘rules’ for genera‐specific bloom development. Based on these models, an expansion in area and/or number of months annually conducive to development of these HABs along the NW European Shelf‐Baltic Sea system and NE Asia was projected for both HAB genera, but no expansion (Prorocentrum spp.), or actual contraction in area and months conducive for blooms (Karenia spp.), was projected in the SE Asian domain. The implications of these projections, especially for Northern Europe, are shifts in vulnerability of coastal systems to HAB events, increased regional HAB impacts to aquaculture, increased risks to human health and ecosystems, and economic consequences of these events due to losses to fisheries and ecosystem services.
Sampling bias inverts ecogeographical relationships in island reptiles
Authors: Ficetola Gentile Francesco , Cagnetta Massimo , Padoa‐Schioppa Emilio , Quas Anita , Razzetti Edoardo , Sindaco Roberto , Bonardi Anna 
Published: June 2014

AbstractAimSpecies richness is one of the commonest measures of biodiversity, and is a basis for analyses at multiple scales. Data quality may affect estimations of species richness, but most broad‐scale studies do not take sampling biases into account. We analysed reptile richness on islands that have received different sampling efforts, and assessed how inventory completeness affects the results of ecogeographical analyses. We also used simulations to evaluate under what circumstances insufficient sampling can bias the outcome of biodiversity analyses.Location Mediterranean islands.MethodsWe gathered data on reptile richness from 974 islands, assuming better sampling in islands with specific inventories. We used Moran's eigenvector mapping to analyse the factors that determine whether an island has been surveyed, and to identify the relationships between reptile richness, geographical parameters and anthropic parameters. We simulated islands, mimicking patterns of true data, and sampled them with varying effort. Simulated richness was analysed using the same approach used for real‐world data.ResultsThe probability that islands were sampled for reptiles was higher in large, human‐populated islands. The relationship between human impact and reptile richness was negative in well‐surveyed islands, but positive in islands that had not been systematically surveyed, because densely populated and accessible islands receive better sampling. In simulations, analyses successfully retrieved the relationships between species richness and human presence only if the average species detection probability was ≥75%. Poorer sampling resulted in biased regression results.Main conclusions Human activities may strongly affect biodiversity, but human presence and accessibility improve sampling effort and thus the quality of biodiversity information. Therefore, regressing known species richness on parameters representing human presence may result in apparent positive relationships. These two facets of human presence (positive on biodiversity knowledge, negative on actual biodiversity) represent a major challenge for ecogeographical studies, as not taking them into account would bias analyses and underestimate human impact.
Fully Screen‐Printed Tunable Microwave Components Based on Optimized Barium Strontium Titanate Thick Films
Authors: Kohler Christian , Nikfalazar Mohammad , Friederich Andreas , Wiens Alex , Sazegar Mohsen , Jakoby Rolf , Binder Joachim R. 
Published: June 2014

The composite system Ba0.6Sr0.4TiO3–ZnO–B2O3 for thick film preparation has been modified via copper–fluorine codoping of BST to make it suitable for the fabrication of co‐fired metal‐insulator‐metal (MIM) components. Based on the resulting improvement of the thick films, MIM varactors and phase shifters were produced by subsequent screen‐printing of silver and BST pastes as well as co‐firing. Microstructural investigations showed the compatibility of silver and BST with neither chemical reaction nor cracking of the layers. The microwave characterization revealed good results regarding tunability and quality factor of the varactors and high figure of merit of 70°/dB at 1.72 GHz for the phase shifter.
Association of better iron status biomarkers and coronary artery disease risk
Authors: Zhou Y. , Liu T. , Kang P. , Jia C. 
Published: June 2014

AbstractBackgroundEpidemiological evidence concerning the role of body iron in coronary artery disease (CAD) is inconsistent, which is largely explained by the lack of relatively ideal estimations of body iron stores.AimThe aim of the present study was to attempt to explore the ideal iron indicator that has the best effect on disease risk for further studies related to iron overload metabolism research worldwide.MethodsA case–control study was conducted with 258 CAD cases and 282 healthy controls. The association of serum iron (SI) parameters, including SI, total iron‐binding capacity (TIBC), serum ferritin (SF) and serum transferrin receptor (sTfR), and CAD risk, was evaluated with receiver operating characteristic analysis. The areas under the receiver operating characteristic curve (AUC) were compared with each other to indicate the one showing the strongest association with CAD risk.ResultsThe AUC (95% confidence interval) were 0.73 (0.69–0.77), 0.74 (0.69–0.78), 0.53 (0.48–0.58) and 0.61 (0.56–0.66) for SI, TIBC, SF and sTfR respectively. After comparing the AUC with each other, the combination of SI and TIBC (AUC (95% confidence interval): 0.86 (0.83–0.90)) was superior to other examined iron parameters or the combination of iron indicators (P < 0.05).ConclusionsThe present study indicated that the combination of SI and TIBC may have the best effect on CAD risk. Further studies are warranted to verify this preliminary result.
Both plasmacytoid dendritic cells and monocytes stimulate natural killer cells early during human herpes simplex virus type 1 infections
Authors: Vogel Karin , Thomann Sabrina , Vogel Benjamin , Schuster Philipp , Schmidt Barbara 
Published: June 2014

SummaryHerpes simplex virus type 1 (HSV‐1), a member of the herpes virus family, is characterized by a short replication cycle, high cytopathogenicity and distinct neurotropism. Primary infection and reactivation may cause severe diseases in immunocompetent and immunosuppressed individuals. This study investigated the role of human plasmacytoid dendritic cells (pDC) in the activation of natural killer (NK) cells for the control of herpesviral infections. Within peripheral blood mononuclear cells, UV‐inactivated HSV‐1 and CpG‐A induced CD69 up‐regulation on NK cells, whereas infectious HSV‐1 was particularly active in inducing NK cell effector functions interferon‐γ (IFN‐γ) secretion and degranulation. The pDC‐derived IFN‐α significantly contributed to NK cell activation, as evident from neutralization and cell depletion experiments. In addition, monocyte‐derived tumour necrosis factor‐α (TNF‐α) induced after exposure to infectious HSV‐1 was found to stimulate IFN‐γ secretion. A minority of monocytes was shown to be non‐productively infected in experiments using fluorescently labelled viruses and quantitative PCR analyses. HSV‐1‐exposed monocytes up‐regulated classical HLA‐ABC and non‐classical HLA‐E molecules at the cell surface in an IFN‐α‐dependent manner, whereas stress molecules MICA/B were not induced. Notably, depletion of monocytes reduced NK cell effector functions induced by infectious HSV‐1 (P < 0·05). Altogether, our data suggest a model in which HSV‐1‐stimulated pDC and monocytes activate NK cells via secretion of IFN‐α and TNF‐α. In addition, infection of monocytes induces NK cell effector functions via TNF‐α‐dependent and TNF‐α‐independent mechanisms. Hence, pDC and monocytes, which are among the first cells infiltrating herpetic lesions, appear to have important bystander functions for NK cells to control these viral infections.
Disruption of macrophage pro‐inflammatory cytokine release in Crohn's disease is associated with reduced optineurin expression in a subset of patients
Authors: Smith Andrew M. , Sewell Gavin W. , Levine Adam P. , Chew Thean S. , Dunne Jenny , O'Shea Nuala R. , Smith Philip J. , Harrison Penelope J. , Macdonald Carol M. , Bloom Stuart L. , Segal Anthony W. 
Published: June 2014

SummaryCrohn's disease (CD) is a complex and highly heterogeneous chronic inflammatory disorder, primarily affecting the gastrointestinal tract. Genetic and functional studies have highlighted a key role for innate immunity in its pathogenesis. Profound systemic defects in innate immunity and acute inflammation are understood to result in markedly delayed clearance of bacteria from the tissues, leading to local chronic granulomatous inflammation and compensatory adaptive immunological changes. Macrophages, key orchestrators of acute inflammation, are likely to play an important role in the initial impaired innate immune response. Monocyte‐derived macrophages from CD patients stimulated with Escherichia coli were shown to release attenuated levels of tumour necrosis factor and interferon‐γ with normal secretion of interleukin‐8 (IL‐8), IL‐10 and IL‐6. In controls, the secretion of these cytokines was strongly positively correlated, which was not seen with CD macrophages. The transcriptomes of CD and control macrophages were examined in an attempt to understand the molecular basis of this defect. There were no differentially expressed genes identified between the two groups, consistent with genetic heterogeneity; however, a number of molecules were found to be under‐expressed in subgroups of CD patients. The most common of these was optineurin (OPTN) which was under‐expressed in approximately 10% of the CD patients. Reduced OPTN expression coincided with lower intracellular protein levels and diminished cytokine secretion after bacterial stimulation both in the patients and with small interfering RNA knockdown in THP‐1 cells. Identifying and studying subgroups of patients with shared defective gene expression could aid our understanding of the mechanisms underlying highly heterogeneous diseases such as CD.
Interleukin‐4 up‐regulation of epidermal interleukin‐19 expression in keratinocytes involves the binding of signal transducer and activator of transcription 6 (Stat6) to the imperfect Stat6 sites
Authors: Bao Lei , Alexander Jaime B. , Shi Vivian Y. , Mohan Girish C. , Chan Lawrence S. 
Published: June 2014

SummaryInterleukin‐19 (IL‐19) plays an important role in asthma by stimulating T helper type 2 (Th2) cytokine production. Interestingly, IL‐4, a key Th2 cytokine, in turn up‐regulates IL‐19 expression in bronchial epithelial cells, so forming a positive feedback loop. In atopic dermatitis (AD), another Th2 disease closely related to asthma, IL‐19 is up‐regulated in the skin. We propose to use IL‐4 transgenic (Tg) mice and human keratinocyte culture to delineate the molecular mechanisms involved in the up‐regulation of IL‐19 in AD. IL‐19 is similarly up‐regulated in the skin of IL‐4 Tg mice as in human AD. Next we show that IL‐4 up‐regulates IL‐19 expression in keratinocytes. Interestingly, the up‐regulation was suppressed by a pan‐Janus kinase (Jak) inhibitor, suggesting that the Jak–signal transducer and activator of transcription (Jak‐STAT) pathway may be involved. Dominant negative studies further indicate that STAT6, but not other STATs, mediates the up‐regulation. Serial 5′ deletion of the IL‐19 promoter and mutagenesis studies demonstrate that IL‐4 up‐regulation of IL‐19 in keratinocytes involves two imperfect STAT6 response elements. Finally, chromatin immunoprecipitation assay studies indicate that IL‐4 increases the binding of STAT6 to its response elements in the IL‐19 promoter. Taken together, we delineate the detailed molecular pathway for IL‐4 up‐regulation of IL‐19 in keratinocytes, which may play an important role in AD pathogenesis.
‘As above, so below’ examining the interplay between emotion and the immune system
Authors: Brod Samuel , Rattazzi Lorenza , Piras Giuseppa , D'Acquisto Fulvio 
Published: June 2014

SummaryWhile the concept of a palpable relationship between our mental and physical well‐being is certainly not new, it is only in the light of modern scientific research that we have begun to realize how deeply connected our emotional and immune states may be. We begin this review with a series of studies demonstrating how four fundamental emotional responses: anger, anxiety, mirth and relaxation are able modulate cytokine production and cellular responses to a variety of immune stimuli. These modulations are shown to be either detrimental or beneficial to a patient's health dependent on the context and duration of the emotion. We also discuss the reverse, highlighting research demonstrating how the loss of key immune cells such as T lymphocytes in clinical and animal studies can negatively impact both emotional well‐being and cognition. Additionally, to give a more complete picture of the manifold pathways that link emotion and the immune system, we give a brief overview of the influence the digestive system has upon mental and immunological health. Finally, throughout this review we attempt to highlight the therapeutic potential of this burgeoning field of research in both the diagnosis and treatment of immune and disorders. As well as identifying some of the key obstacles the field must address in order to put this potential into practice.
‘Default’ generated neonatal regulatory T cells are hypomethylated at conserved non‐coding sequence 2 and promote long‐term cardiac allograft survival
Authors: Cheng Chao , Wang Sihua , Ye Ping , Huang Xiaofan , Liu Zheng , Wu Jie , Sun Yuan , Xie Aini , Wang Guohua , Xia Jiahong 
Published: June 2014

SummaryRegulatory T (Treg) cells play an important role in the maintenance of immune self‐tolerance and homeostasis. We previously reported that neonatal CD4+ T cells have an intrinsic ‘default’ mechanism to become Treg (neoTreg) cells in response to T‐cell receptor (TCR) stimulation. However, the underlying mechanisms are unclear and the effects of neoTreg cells on regulating immune responses remain unknown. Due to their involvement in Foxp3 regulation, we examined the role of DNA methyltransferase 1 (DNMT1) and DNMT3b during the induction of neoTreg cells in the Foxp3gfp mice. The function of neoTreg cells was assessed in an acute allograft rejection model established in RAG2−/− mice with allograft cardiac transplantation and transferred with syngeneic CD4+ effector T cells. Following ex vivo TCR stimulation, the DNMT activity was increased threefold in adult CD4+ T cells, but not significantly increased in neonatal cells. However, adoptively transferred neoTreg cells significantly prolonged cardiac allograft survival (mean survival time 47 days, P < 0·001) and maintained Foxp3 expression similar to natural Treg cells. The neoTreg cells were hypomethylated at the conserved non‐coding DNA sequence 2 locus of Foxp3 compared with adult Treg cells. The DNMT antagonist 5‐aza‐2′‐deoxycytidine (5‐Aza) induced increased Foxp3 expression in mature CD4+ T cells. 5‐Aza‐inducible Treg cells combined with continuous 5‐Aza treatment prolonged graft survival. These results indicate that the ‘default’ pathway of neoTreg cell differentiation is associated with reduced DNMT1 and DNMT3b response to TCR stimulus. The neoTreg cells may be a strategy to alleviate acute allograft rejection.
Mitochondrial DNA diversity of Anatolian indigenous domestic goats
Authors: Akis I. , Oztabak K. , Mengi A. , Un C. 
Published: June 2014

SummaryAnatolia has been an important region for civilizations and agricultural revolution as a major domestication centre for livestock species. Goats (Capra hircus) were among the earliest domesticated animals in this region. In this study, genetic diversity of Anatolian goat breeds was characterized by comparison of mitochondrial DNA hypervariable region 1. A total of 295 individuals, including 99 Anatolian Black goats, 96 Angora goats and 100 Kilis goats, were used. Haplogroup A was found to be the dominant haplogroup in all three breeds. The highest haplogroup diversity, including haplogroups A, B2, C and G, was observed in the Anatolian Black breed. Haplogroup D was only observed in Kilis and Angora goats. Haplogroup G was found in Angora and Anatolian Black breeds. The Anatolian goat breeds had high genetic diversity values and a weak phylogeographical structure. The nucleotide diversity values were found to be higher than those in previously studied goat breeds. The fact that Anatolia is a domestication centre and its geographical position as a junction of trade routes may have caused the higher genetic diversity of Anatolian goat breeds.
Effect and cardiovascular safety of adding rosiglitazone to insulin therapy in type 2 diabetes: A meta‐analysis
Authors: Lu Yu , Ma Delin , Xu Weijie , Shao Shiying , Yu Xuefeng 
Published: June 2014

AbstractAims/IntroductionRecently, the use of rosiglitazone has been limited or withdrawn from the market as a result of cardiovascular risk. However, theoretically adding rosiglitazone to insulin could help insulin to decrease the glucose level. The present meta‐analysis was designed to investigate the effect and safety of adding rosiglitazone to insulin therapy in type 2 diabetes.Materials and MethodsWe searched published and unpublished databases through to March 2012. Randomized controlled trials (RCTs) comparing rosiglitazone in combination with insulin (RSG + INS) vs insulin alone (INS) in type 2 diabetes with outcomes including glycated hemoglobin levels, insulin dose, lipid parameters, blood pressure, edema and cardiovascular adverse events were selected.ResultsNine RCTs with durations of 24–26 weeks involving 1,916 patients were included. The RSG + INS group showed significantly decreased glycated hemoglobin levels by 0.89% (P < 0.00001) with an 8.48‐U reduction in daily insulin dose (P <0.00001). However, the risks of hypoglycemia and edema were more frequent in the RSG+INS group (P < 0.0001; P = 0.03, respectively). Total cholesterol level was significantly increased in the RSG+INS group (P < 0.00001), but none of the high‐density lipoprotein cholesterol, low‐density lipoprotein cholesterol, very low‐density lipoprotein cholesterol or triglyceride levels were significantly different between groups. There were no significant differences between groups with regard to the risks of myocardial infarction, heart failure, cardiovascular death or all‐cause death.ConclusionsRosiglitazone could help type 2 diabetes patients with poorly controlled glucose with insulin therapy to decrease glucose levels and reduce their daily insulin dose, but at the cost of increased total cholesterol level, hypoglycemia and edema risk. Compared with insulin therapy, adding rosiglitazone to insulin did not increase the risks of myocardial infarction, heart failure, cardiovascular death or all‐cause death.
Effect of a state‐based incentive programme on the use of electronic health records
Authors: Vest Joshua R. , Kern Lisa M. , Abramson Erika , Ancker Jessica S. , Kaushal Rainu ,   HITEC Investigators
Published: June 2014

AbstractRationale, aims and objectivesIn 2004, New York passed the Health Care Efficiency and Affordability Law for New Yorkers (HEAL NY) Capital Grants Program, which was the largest state‐based investment in health information technology adoption in the United States. We sought to evaluate the effects of this programme on electronic health records (EHR) usage.MethodsWe undertook a case‐control study of health care providers who had signed up with a regional extension centre, some of whom had also received HEAL funding through programmes intended to support EHR adoption. The outcome of interest was achievement of Medicare or Medicaid Meaningful Use and the primary exposure was any link to HEAL NY funding. The association between Meaningful Use status and independent variables was measured using logistic regression models.ResultsMeaningful Users were more likely to have had a history of HEAL NY funding (OR = 1.83; 95% CI = 1.59, 2.09). Also, achievement of Meaningful Use was associated with having an EHR before 2011 (OR = 1.64; 95% CI = 146, 1.83). Among those with EHRs prior to 2011, the odds of achieving Meaningful Use were statistically higher if coupled with HEAL NY funding (OR = 3.12; 95% CI = 2.50, 3.90).ConclusionAchieving Meaningful Use was associated with a history of HEAL NY funding. However, it was the combination of HEAL NY funding and historic usage of EHRs that was associated with the largest increase in the odds that the provider was a Meaningful User. These findings indicate that state‐based incentive programmes can support the effective usage of health
information technologies.