bluuebunny/crossref_metadata_2025_split huggingface dataset:
Disentangling tree species identity and richness effects on the herb layer: first results from a German tree diversity experiment
Authors: Ampoorter Evy , Baeten Lander , Vanhellemont Margot , Bruelheide Helge , Scherer‐Lorenzen Michael , Baasch Annett , Erfmeier Alexandra , Hock Maria , Verheyen Kris 
Published: March 2015

AbstractQuestionsThe forest herb layer provides a multitude of ecosystem services as a result of its species‐rich character. Herb layer diversity and biomass are both influenced by tree layer composition and species richness through species‐specific influences on environmental conditions. The results of observational studies on richness–biomass relationships between tree and herb layer have not been unequivocal. We examined tree species identity and richness effects on herb layer species richness, composition, biomass and nutrient concentrations in young experimental tree plantations.LocationBIOTREE tree diversity experiment, Kaltenborn, Germany.MethodsSixteen plots were planted in 2004, using a pool of four tree species (beech, oak, Douglas‐fir, Norway spruce) and four richness levels, comprised of all possible species combinations. In this way, complete dilution was avoided, allowing separation of tree species identity and richness effects. Mixed plots consisted of a matrix of monospecific patches. One permanent vegetation quadrat of 1 m2was established in the centre of four patches per plot. The herb layer was monitored in 2004 and 2010; in 2010 light measurements were performed in each quadrat, and in 2011 above‐ground biomass was sampled on 0.25 m2within the quadrat.ResultsCommunity composition shifted markedly between 2004 and 2010. Tree species identity did not yet influence temporal compositional turnover or herb layer species richness in 2004 and 2010. Ellenberg N indicated a temporal shift towards lower soil fertility under all tree species, whereas Ellenberg R indicated decreasing soil acidity under beech and Douglas‐fir. Ellenberg L and F showed no shift from 2004 to 2010. Apart from the significantly lower Ellenberg N for beech, none of the Ellenberg indicators indicated interspecific differences. Douglas‐fir, and especially Norway spruce, negatively influenced total above‐ground herb layer biomass. Douglas‐fir also induced lower relative light availability, higher potassium, magnesium and nitrogen concentrations and lower carbon:nitrogen ratios in the total biomass. Higher tree species richness positively affected graminoid and total biomass and also slightly increased plot‐level herb layer species richness.ConclusionsDespite the young age of the experiment, tree species identity and richness effects on the herb layer could be discerned. We expect these relations to become stronger with time.
Ecology and genetic variation of Amblyomma tonelliae in Argentina
Authors: TARRAGONA E. L. , MANGOLD A. J. , MASTROPAOLO M. , GUGLIELMONE A. A. , NAVA S. 
Published: March 2015

AbstractThe ecology of Amblyomma tonelliae (Ixodida: Ixodidae), including its seasonal distribution and the development periods of each stage, was investigated during a study carried out over two consecutive years in northwestern Argentina. In addition, the genetic variation of this tick was studied through analyses of 16S rDNA sequences. Amblyomma tonelliae has a 1‐year lifecycle characterized by a long pre‐moult period in larvae with no development of morphogenetic diapause. Larvae peak in abundance during late autumn and early winter; nymphs peak in abundance in spring, and adults do so from late spring to early summer. Amblyomma tonelliae shows a marked ecological preference for the driest areas of the Chaco ecoregion. In analyses of 16S rDNA sequences in genes from different populations of A. tonelliae, values for nucleotide diversity and the average number of nucleotide differences showed genetic diversity within this species to be low. No significant differences were found in comparisons among populations.
A critical evaluation of whether recombination in virus‐resistant transgenic plants will lead to the emergence of novel viral diseases
Authors: Tepfer Mark , Jacquemond Mireille , García‐Arenal Fernando 
Published: March 2015

SummaryIn the evaluation of the potential impacts of first‐generation genetically modified (GM) crops, one of the most complex issues has been whether the expression of viral sequences would lead to the emergence of novel viruses, which could occur through recombination between transgene mRNA and that of an infecting non‐target virus. Here, we examine this issue, focusing on Cucumber mosaic virus (CMV), which is a particularly pertinent choice, as it is both a major plant pathogen and also the virus with which this question has been studied in the most detail. Using recent results on recombination in CMV, we employ a novel framework giving particular prominence to the formulation of the risk hypothesis and to hypothesis testing via examination of the potential pathway to harm. This allows us to conclude with greater certainty that the likelihood of this potential harm, the emergence of novel viruses, is low.
Changes in intracuff pressure of a cuffed endotracheal tube during surgery for congenital heart disease using cardiopulmonary bypass
Authors: Kako Hiromi , Alkhatib Omar , Krishna Senthil G. , Khan Sarah , Naguib Aymen , Tobias Joseph D. 
Published: March 2015

SummaryBackgroundWith the development of newer polyurethane cuffed endotracheal tubes (cETTs), there has been a shift in clinical practice among pediatric anesthesiologists. Despite improvements in design, excessive inflation of the cuff can still compromise tracheal mucosal perfusion. Several perioperative factors can affect the intracuff pressure (CP), and there is no consensus on safe CP in pediatric patients undergoing repair of congenital cardiac disease (CHD) utilizing cardiopulmonary bypass (CPB). In the current study, the CP was continuously monitored in pediatric patients undergoing surgery for CHD.MethodsAfter IRB approval, this observational study was conducted on pediatric patients who underwent repair of CHD using CPB with a cETT in place. After anesthetic induction and endotracheal intubation, the cuff was inflated using the air leak technique while maintaining a continuous positive airway pressure of 20 cmH2O. After inflation, the CP was continuously monitored throughout the procedure. In addition, temperature and mean arterial pressure (MAP) were also recorded.ResultsThe study included 33 patients who ranged in age from 1 month to 15.3 years. Their weight ranged from 4.0 to 83.6 kg. Six patients were excluded from the analysis due to the need to add or remove air from the cuff, leaving 27 patients for data analysis for cuff pressure over time. The baseline CP at the time of inflation was 16.1 ± 7.6 cmH2O. With the use of CPB and initiation of hypothermia, when compared to the baseline, the CP decreased by −0.7 ± 5.8 cmH2O at 35–37°C, −9.1 ± 8.4 cmH2O at 31–33°C, −7.8 ± 6.2 cmH2O at 27–29°C, and −11.1 ± 6.0 cmH2O at <27°C. With rewarming, the CP increased back to the baseline level (−3.5 ± 7.0 cmH2O).ConclusionThere was a significant decrease in the CP during CPB and associated hypothermia. This may offer some protection for mucosal perfusion during CPB which is usually associated with lower than normal MAP. However, the decrease in the CP may compromise the tracheal seal which may not offer the intended protection for the airway from aspiration.
Host‐induced gene silencing of an essential chitin synthase gene confers durable resistance to Fusarium head blight and seedling blight in wheat
Authors: Cheng Wei , Song Xiu‐Shi , Li He‐Ping , Cao Le‐Hui , Sun Ke , Qiu Xiao‐Li , Xu Yu‐Bin , Yang Peng , Huang Tao , Zhang Jing‐Bo , Qu Bo , Liao Yu‐Cai 
Published: March 2015

SummaryFusarium head blight (FHB) and Fusarium seedling blight (FSB) of wheat, caused by Fusarium pathogens, are devastating diseases worldwide. We report the expression of RNA interference (RNAi) sequences derived from an essential Fusarium graminearum (Fg) virulence gene, chitin synthase (Chs) 3b, as a method to enhance resistance of wheat plants to fungal pathogens. Deletion of Chs3b was lethal to Fg; disruption of the other Chs gene family members generated knockout mutants with diverse impacts on Fg. Comparative expression analyses revealed that among the Chs gene family members, Chs3b had the highest expression levels during Fg colonization of wheat. Three hairpin RNAi constructs corresponding to the different regions of Chs3b were found to silence Chs3b in transgenic Fg strains. Co‐expression of these three RNAi constructs in two independent elite wheat cultivar transgenic lines conferred high levels of stable, consistent resistance (combined type I and II resistance) to both FHB and FSB throughout the T3 to T5 generations. Confocal microscopy revealed profoundly restricted mycelia in Fg‐infected transgenic wheat plants. Presence of the three specific short interfering RNAs in transgenic wheat plants was confirmed by Northern blotting, and these RNAs efficiently down‐regulated Chs3b in the colonizing Fusarium pathogens on wheat seedlings and spikes. Our results demonstrate that host‐induced gene silencing of an essential fungal chitin synthase gene is an effective strategy for enhancing resistance in crop plants under field test conditions.
The Exchange Rate Dimension of Inflation Targeting: Target Levels and Currency Volatility
Authors: Du Plessis Stan , Reid Monique Brigitte 
Published: March 2015

AbstractThe surprising volatility of floating exchange rates have puzzled macroeconomists and challenged policy makers since the seventies. This is no less true in South Arica where the Rand's volatility is a longstanding policy and business challenge. This paper extends the literature on nominal and institutional factors associated with currency volatility. Rose's description of inflation as “Bretton Woods in reverse” is the departure point and is read with Berganza and Broto's recent demonstration in a time series study that inflation targeting emerging market economies have experience higher exchange rate volatility. Meanwhile Bleaney and Tian have shown the cross‐sectional connection between the level of inflation and exchange rate volatility. We build on Bleaney and Tian's cross‐sectional approach to investigate the association between the level at which inflation targeting countries target inflation and exchange rate volatility over the long run. Crucially, we control for the average level of inflation and distinguish between inflation targeting countries that target high and low levels of inflation, in order to investigate whether the choice of the level of the inflation target (an institutional feature) is associated with greater exchange rate volatility.
Shigella flexneri Regulation of ARF6 Activation during Bacterial Entry via an IpgD-Mediated Positive Feedback Loop
Authors: Garza-Mayers Anna Cristina , Miller Kelly A. , Russo Brian C. , Nagda Dipal V. , Goldberg Marcia B. 
Published: March 2015

ABSTRACT
Entry into cells is critical for virulence of the human bacterial pathogens Shigella spp. Shigella spp. induce membrane ruffle formation and macropinocytic uptake, but the events instigating this process are incompletely understood. The host small GTPase ADP-ribosylation factor 6 (ARF6) functions in membrane trafficking at the plasma membrane and activates membrane ruffle formation. We demonstrate that ARF6 is required for efficient Shigella flexneri entry, is activated by S. flexneri dependent on the phosphatase activity of the type III secreted effector IpgD, and depends on cytohesin guanine nucleotide exchange factors (GEFs) for recruitment to entry sites. The cytohesin GEF ARF nucleotide binding site opener (ARNO) is recruited to these sites, also dependent on IpgD phosphatase activity. ARNO recruitment is independent of ARF6, indicating that, in addition to the described recruitment of ARNO by ARF6, ARNO is recruited upstream of ARF6. Our data provide evidence that ARF6, IpgD, phosphoinositide species, and ARNO constitute a previously undescribed positive feedback loop that amplifies ARF6 activation at bacterial entry sites, thereby promoting efficient S. flexneri uptake.

IMPORTANCE
Shigella spp. cause diarrhea and dysentery by infection of epithelial cells in the human colon. Critical to disease is the ability of Shigella to enter into cells, yet the mechanisms involved in entry are incompletely understood. We demonstrate that the small GTPase ADP-ribosylation factor 6 (ARF6) is required for efficient cellular entry of Shigella flexneri and that activation of ARF6 depends on the phosphatase activity of the Shigella protein IpgD, which is introduced into cells via the bacterial type III secretion system. We further show that IpgD phosphatase activity is required for recruitment of the ARF6 guanine nucleotide exchange factor (GEF) ARF nucleotide binding site opener (ARNO) to bacterial entry sites and that ARNO lies upstream of ARF6 activation. These relationships define a positive feedback loop that contributes to activation of ARF6 at S. flexneri entry sites and leads to local amplification of signals that promote bacterial entry.
Does neighbourhood composition modify the association between acculturation and unhealthy dietary behaviours?
Authors: Zhang Donglan , Meijgaard Jeroen van , Shi Lu , Cole Brian , Fielding Jonathan 
Published: March 2015

ObjectiveStudies have shown that immigrants’ acculturation is associated with numerous unhealthy behaviours. Yet, the role of environmental factors in modifying the effect of acculturation on health behaviours has received little attention. This study aims to create a more nuanced understanding of the health effects of acculturation by examining how neighbourhood immigrant composition modifies the association between individuals’ eating patterns and acculturation.MethodsCross-sectional Data from Los Angeles County Health Survey 2007 adult sample were linked to data on retail food establishments and US Census 2000 neighbourhood characteristics. Acculturation was measured by language spoken at home and years stayed in the US. Eating fast food more than once per week and eating zero serving of fruit or vegetables during the previous day were used as proxy indicators for unhealthy dietary behaviour. Multilevel logistic regression models were performed in the full sample and in the sample with only Latino adults.ResultsImmigrants’ lack of acculturation and living in a neighbourhood with a high percentage immigrants were associated with healthier dietary behaviour. We also identified that lack of acculturation conveyed a significantly stronger protective effect on regular fast-food consumption for immigrants living in neighbourhoods with higher percentage immigrants (OR: 0.34, 95% CI: 0.12 to 0.93).ConclusionsAmong immigrants in Los Angeles County, living in a neighbourhood with a high density of other immigrants attenuates the negative effects of acculturation on healthy eating behaviours. Healthy eating promotion efforts should build on this protective effect in outreach to acculturating immigrant communities.
Microbial communities and their primary to early diagenetic mineral phases; the record from Neoproterozoic microbialites of Qarn Alam, Oman
Authors: Mettraux M. , Homewood P. , Dos Anjos C. , Erthal M. , Lima R. , Matsuda N. , Souza A. , Al Balushi S. 
Published: March 2015

Abstract
The 10 m-scale shallowing-up Neoproterozoic carbonate cycles at Qarn Alam (Oman) provide a record of microbial textures and the communities responsible for them. This is documented for four major microbialite facies. Despite their age, these microbialites show extremely fine preservation of microbial fossils and mineral associations (primary calcite and dolomite with minor phosphate, glauconite, palygorskite, hematite and goethite) and they are the record of a suite of microbial communities, from pellicular biofilms (planar laminites) to mats and gels (crinkly laminites, and stromatolitic layered and massive thrombolites) and a more complex microbial community in bushy thrombolites possibly involving a sponge-like form. Mineralized extra-cellular polymeric substances (EPS) resembles that of modern microbial mats. The mineral associations, as well as cathodoluminescence attributes, indicate oxic to suboxic conditions during deposition and early diagenesis for planar laminites and crinkly laminites, but more evaporitic to saline conditions during development of thrombolites of the upper part of a cycle. Early cementation under variable redox conditions sealed the organomineralized phases.
Prevention of Carcinogen and Inflammation-Induced Dermal Cancer by Oral Rapamycin Includes Reducing Genetic Damage
Authors: Dao Vinh , Pandeswara Srilakshmi , Liu Yang , Hurez Vincent , Dodds Sherry , Callaway Danielle , Liu Aijie , Hasty Paul , Sharp Zelton D. , Curiel Tyler J. 
Published: March 2015

Abstract
Cancer prevention is a cost-effective alternative to treatment. In mice, the mTOR inhibitor rapamycin prevents distinct spontaneous, noninflammatory cancers, making it a candidate broad-spectrum cancer prevention agent. We now show that oral microencapsulated rapamycin (eRapa) prevents skin cancer in dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA) carcinogen-induced, inflammation-driven carcinogenesis. eRapa given before DMBA/TPA exposure significantly increased tumor latency, reduced papilloma prevalence and numbers, and completely inhibited malignant degeneration into squamous cell carcinoma. Rapamycin is primarily an mTORC1-specific inhibitor, but eRapa did not reduce mTORC1 signaling in skin or papillomas, and did not reduce important proinflammatory factors in this model, including p-Stat3, IL17A, IL23, IL12, IL1β, IL6, or TNFα. In support of lack of mTORC1 inhibition, eRapa did not reduce numbers or proliferation of CD45−CD34+CD49fmid skin cancer initiating stem cells in vivo and marginally reduced epidermal hyperplasia. Interestingly, eRapa reduced DMBA/TPA-induced skin DNA damage and the hras codon 61 mutation that specifically drives carcinogenesis in this model, suggesting reduction of DNA damage as a cancer prevention mechanism. In support, cancer prevention and DNA damage reduction effects were lost when eRapa was given after DMBA-induced DNA damage in vivo. eRapa afforded picomolar concentrations of rapamycin in skin of DMBA/TPA-exposed mice, concentrations that also reduced DMBA-induced DNA damage in mouse and human fibroblasts in vitro. Thus, we have identified DNA damage reduction as a novel mechanism by which rapamycin can prevent cancer, which could lay the foundation for its use as a cancer prevention agent in selected human populations. Cancer Prev Res; 8(5); 400–9. ©2015 AACR.
Loss of MIG6 Accelerates Initiation and Progression of Mutant Epidermal Growth Factor Receptor–Driven Lung Adenocarcinoma
Authors: Maity Tapan K. , Venugopalan Abhilash , Linnoila Ilona , Cultraro Constance M. , Giannakou Andreas , Nemati Roxanne , Zhang Xu , Webster Joshua D. , Ritt Daniel , Ghosal Sarani , Hoschuetzky Heinz , Simpson R. Mark , Biswas Romi , Politi Katerina , Morrison Deborah K. , Varmus Harold E. , Guha Udayan 
Published: March 2015

AbstractSomatic mutations in the EGFR kinase domain drive lung adenocarcinoma. We have previously identified MIG6, an inhibitor of ERBB signaling and a potential tumor suppressor, as a target for phosphorylation by mutant EGFRs. Here, we demonstrate that MIG6 is a tumor suppressor for the initiation and progression of mutant EGFR–driven lung adenocarcinoma in mouse models. Mutant EGFR–induced lung tumor formation was accelerated in Mig6-deficient mice, even with Mig6 haploinsufficiency. We demonstrate that constitutive phosphorylation of MIG6 at Y394/Y395 in EGFR-mutant human lung adenocarcinoma cell lines is associated with an increased interaction of MIG6 with mutant EGFR, which may stabilize EGFR protein. MIG6 also fails to promote mutant EGFR degradation. We propose a model whereby increased tyrosine phosphorylation of MIG6 decreases its capacity to inhibit mutant EGFR. Nonetheless, the residual inhibition is sufficient for MIG6 to delay mutant EGFR–driven tumor initiation and progression in mouse models.Significance: This study demonstrates that MIG6 is a potent tumor suppressor for mutant EGFR–driven lung tumor initiation and progression in mice and provides a possible mechanism by which mutant EGFR can partially circumvent this tumor suppressor in human lung adenocarcinoma. Cancer Discov; 5(5); 534–49. ©2015 AACR.See related commentary by Izumchenko and Sidransky, p. 472.This article is highlighted in the In This Issue feature, p. 453
IFNγ Induces DNA Methylation–Silenced GPR109A Expression via pSTAT1/p300 and H3K18 Acetylation in Colon Cancer
Authors: Bardhan Kankana , Paschall Amy V. , Yang Dafeng , Chen May R. , Simon Priscilla S. , Bhutia Yangzom D. , Martin Pamela M. , Thangaraju Muthusamy , Browning Darren D. , Ganapathy Vadivel , Heaton Christopher M. , Gu Keni , Lee Jeffrey R. , Liu Kebin 
Published: March 2015

Abstract
Short-chain fatty acids, metabolites produced by colonic microbiota from fermentation of dietary fiber, act as anti-inflammatory agents in the intestinal tract to suppress proinflammatory diseases. GPR109A is the receptor for short-chain fatty acids. The functions of GPR109A have been the subject of extensive studies; however, the molecular mechanisms underlying GPR109A expression is largely unknown. We show that GPR109A is highly expressed in normal human colon tissues, but is silenced in human colon carcinoma cells. The GPR109A promoter DNA is methylated in human colon carcinoma. Strikingly, we observed that IFNγ, a cytokine secreted by activated T cells, activates GPR109A transcription without altering its promoter DNA methylation. Colon carcinoma grows significantly faster in IFNγ-deficient mice than in wild-type mice in an orthotopic colon cancer mouse model. A positive correlation was observed between GPR109A protein level and tumor-infiltrating T cells in human colon carcinoma specimens, and IFNγ expression level is higher in human colon carcinoma tissues than in normal colon tissues. We further demonstrated that IFNγ rapidly activates pSTAT1 that binds to the promoter of p300 to activate its transcription. p300 then binds to the GPR109A promoter to induce H3K18 hyperacetylation, resulting in chromatin remodeling in the methylated GPR109A promoter. The IFNγ-activated pSTAT1 then directly binds to the methylated but hyperacetylated GPR109 promoter to activate its transcription. Overall, our data indicate that GPR109A acts as a tumor suppressor in colon cancer, and the host immune system might use IFNγ to counteract DNA methylation–mediated GPR109A silencing as a mechanism to suppress tumor development. Cancer Immunol Res; 3(7); 795–805. ©2015 AACR.