bluuebunny/crossref_metadata_2025_split huggingface dataset:
Glucocorticoid signaling regulates cell invasion and migration in the human first‐trimester trophoblast cell line Sw.71
Authors: Kisanga Edwina P. , Tang Zhonghua , Guller Seth , Whirledge Shannon 
Published: May 2018

ProblemThe development of the placenta and its functions are sensitive to infection and stress, which can activate the hypothalamic‐pituitary‐adrenal axis. Adrenally produced glucocorticoids are the body's primary mediators of the inflammatory and stress response. Although the glucocorticoid receptor (GR) is expressed in all human villous trophoblast tissue, the effect of glucocorticoids on placentation is not well understood.Method of studyUsing microarray analysis, we identified the glucocorticoid‐regulated transcriptional profile in the immortalized first‐trimester extravillous trophoblast cell line Swan.71 (Sw.71).ResultsThe synthetic glucocorticoid dexamethasone significantly regulated 3829 genes, including genes associated with cell movement, growth, and survival. SERPINE1, an inhibitor of trophoblast invasion, was induced by glucocorticoids in Sw.71 cells and is associated with the pathogenesis of preeclampsia. Glucocorticoid treatment induced recruitment of activated polymerase II and GR to the SERPINE1 promoter, suggesting a mechanism for transcriptional regulation. Functionally, glucocorticoid treatment inhibited cell proliferation, migration, and invasion.ConclusionThese findings suggest that glucocorticoids regulate extravillous trophoblast functions by altering the gene expression profile, which may contribute to the pathogenesis of reproductive disorders such as preeclampsia and IUGR.
Extracorporeal Membrane Oxygenation Characteristics and Outcomes in Adult Patients With Down Syndrome
Authors: Duffy Vicky , Gomez Daniel , Rycus Peter , Rivera Brian , Santoro Stephanie L , Backes Carl H , Cua Clifford L 
Published: May 2018

AbstractPatients with Down syndrome (DS) may have multiple medical issues that place them at risk for requiring extracorporeal membrane oxygenation. Use of extracorporeal membrane oxygenation in pediatric patients with Down syndrome has been described, but minimal data exist for extracorporeal membrane oxygenation use in adults with Down syndrome. The goal of this study was to describe the clinical characteristics and to determine if there were differences between adult extracorporeal membrane oxygenation patients with Down syndrome that were alive (aDS) versus those that died (dDS) prior to hospital discharge. Patients with Down syndrome that were 18 years and older registered in the Extracorporeal Life Support Organization registry from 1983 to 2016 were analyzed. Demographics and extracorporeal membrane oxygenation characteristics were recorded. A total of 21 adults with Down syndrome were identified. Incidence of extracorporeal membrane oxygenation in adults with Down syndrome was 0.88 per 1000 extracorporeal membrane oxygenation procedures. Hospital mortality was 57.1% (12/21). There were no significant differences between aDS versus dDS for age (24.9 ± 4.8 vs. 28.1 ± 10.2 years), weight (90.7 ± 13.0 vs. 79.1 ± 27.0 kg), gender (4 males vs. 8 males), initial pH (7.18 ± 0.19 vs. 7.27 ± 0.16), or initial pO2 (51.7 ± 13.9 vs. 45.4 ± 19.9), respectively. There were no significant differences between aDS versus dDS in duration of extracorporeal membrane oxygenation run (239 ± 159 h vs. 455 ± 570 h, respectively), ventilator or extracorporeal membrane oxygenation mode, and nitric oxide use. aDS had fewer incidences of mechanical and neurologic complications (41.7% vs. 0.0%, P < 0.05) versus dDS. There were no other significant differences in complication rates between the two groups. Use of extracorporeal membrane oxygenation in the adult population with Down syndrome is significantly less compared to the pediatric population with Down syndrome. Baseline characteristics are not predictive of overall survival. There were minimal differences noted between aDS versus dDS during their extracorporeal membrane oxygenation course. Mortality rates are similar to non‐Down syndrome patients placed on extracorporeal membrane oxygenation. Extracorporeal membrane oxygenation may be a reasonable option for adult patients with Down syndrome requiring intensive care.
Programmed necrosis in cardiomyocytes: mitochondria, death receptors and beyond
Authors: Zhang Junxia , Liu Dairu , Zhang Mao , Zhang Yan 
Published: May 2018

Excessive death of cardiac myocytes leads to many cardiac diseases, including myocardial infarction, arrhythmia, heart failure and sudden cardiac death. For the last several decades, most work on cell death has focused on apoptosis, which is generally considered as the only form of regulated cell death, whereas necrosis has been regarded to be an unregulated process. Recent findings reveal that necrosis also occurs in a regulated manner and that it is closely related to the physiology and pathophysiology of many organs, including the heart. The recognition of necrosis as a regulated process mandates a re‐examination of cell death in the heart together with the mechanisms and therapy of cardiac diseases. In this study, we summarize the regulatory mechanisms of the programmed necrosis of cardiomyocytes, that is, the intrinsic (mitochondrial) and extrinsic (death receptor) pathways. Furthermore, the role of this programmed necrosis in various heart diseases is also delineated. Finally, we describe the currently known pharmacological inhibitors of several of the key regulatory molecules of regulated cell necrosis and the opportunities for their therapeutic use in cardiac disease. We intend to systemically summarize the recent progresses in the regulation and pathological significance of programmed cardiomyocyte necrosis along with its potential therapeutic applications to cardiac diseases.Linked ArticlesThis article is part of a themed section on Mitochondrial Pharmacology: Featured Mechanisms and Approaches for Therapy Translation. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.22/issuetoc
Human monocyte transcriptional profiling identifies IL‐18 receptor accessory protein and lactoferrin as novel immune targets in hypertension
Authors: Alexander Matthew R , Norlander Allison E , Elijovich Fernando , Atreya Ravi V , Gaye Amadou , Gnecco Juan S , Laffer Cheryl L , Galindo Cristi L , Madhur Meena S 
Published: May 2018

Background and PurposeMonocytes play a critical role in hypertension. The purpose of our study was to use an unbiased approach to determine whether hypertensive individuals on conventional therapy exhibit an altered monocyte gene expression profile and to perform validation studies of selected genes to identify novel therapeutic targets for hypertension.Experimental ApproachNext generation RNA sequencing identified differentially expressed genes in a small discovery cohort of normotensive and hypertensive individuals. Several of these genes were further investigated for association with hypertension in multiple validation cohorts using qRT‐PCR, regression analysis, phenome‐wide association study and case–control analysis of a missense polymorphism.Key ResultsWe identified 60 genes that were significantly differentially expressed in hypertensive monocytes, many of which are related to IL‐1β. Uni‐ and multivariate regression analyses of the expression of these genes with mean arterial pressure (MAP) revealed four genes that significantly correlated with MAP in normotensive and/or hypertensive individuals. Of these, lactoferrin (LTF), peptidoglycan recognition protein 1 and IL‐18 receptor accessory protein (IL18RAP) remained significantly elevated in peripheral monocytes of hypertensive individuals in a separate validation cohort. Interestingly, IL18RAP expression associated with MAP in a cohort of African Americans. Furthermore, homozygosity for a missense single nucleotide polymorphism in LTF that decreases antimicrobial function and increases protein levels (rs1126478) was over‐represented in patients with hypertension relative to controls (odds ratio 1.16).Conclusions and ImplicationsThese data demonstrate that monocytes exhibit enhanced pro‐inflammatory gene expression in hypertensive individuals and identify IL18RAP and LTF as potential novel mediators of human hypertension.Linked ArticlesThis article is part of a themed section on Immune Targets in Hypertension. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.12/issuetoc
Retrotransposable genetic elements causing neutrophil defects
Authors: Roos Dirk , de Boer Martin 
Published: May 2018

AbstractBackgroundRetrotransposable elements are stretches of DNA that encode proteins with the inherent ability to insert their own RNA or another RNA by reverse transcriptase as DNA into a new genomic location. In humans, the only autonomous retrotransposable elements are members of the Long INterspersed Element‐1 (LINE‐1) family. LINE‐1s may cause gene inactivation and human disease.DesignWe present a brief summary of the published knowledge about LINE‐1s in humans and the RNAs that these elements can transpose, and we focus on the effect of LINE‐1‐mediated retrotransposition on human neutrophil function.ResultsRetrotransposons can cause genetic disease by two primary mechanisms: (1) insertional mutagenesis and (2) nonallelic homologous recombination. The only known neutrophil function affected by retrotransposition is that of NADPH oxidase activity. Four patients with chronic granulomatous disease (CGD) are known with LINE‐1‐mediated insertional inactivation of CYBB, the gene that encodes the gp91phox component of the phagocyte NADPH oxidase. In addition, 5 CGD patients had a large deletion in the NCF2 gene, encoding the p67phox component, and 2 CGD patients had a similar deletion in NCF1, encoding p47phox. These deletions were caused by nonallelic homologous recombination between 2 Alu elements at the borders of each deletion. Alu elements have spread throughout the human genome by LINE‐1 retrotransposition.ConclusionsProbably, the occurrence of LINE‐1‐mediated insertions causing autosomal CGD has been underestimated. It might be worthwhile to reinvestigate the DNA from autosomal CGD patients with missplice mutations and large deletions for indications of LINE‐1‐mediated insertions.
Nutrient transfer supports a beneficial relationship between the canopy ant,Azteca trigona, and its host tree
Authors: Lucas Jane M. , Clay Natalie A. , Kaspari Michael 
Published: May 2018

1. Energy fluxes between ants and plants have been a focal point for documenting mutualistic behaviour. Plants can provide resources to ants through the production of extrafloral nectaries. In exchange, ants can fertilise plants through their nutrient‐ and microbe‐rich refuse.2. Here, we test a potential facultative mutualism between the carton‐nesting canopy ant,Azteca trigona, and their host trees. Through observational and experimental approaches, this study documents how nutrient transfer provides a basis for this beneficial ant–plant relationship.3. In a greenhouse experiment, fertilisation with sterilised refuse (i.e. nutrients only) increased seedling growth three‐fold, while the refuse with its natural microbial community increased growth 11‐fold.4. Total root density was doubled in refuse piles compared with the surrounding areain situ. On average, refuse provides host trees and the surrounding plant community with access to a > 800% increase in N, P and K relative to leaf litter.5.Azteca trigonapreferentially nests in trees with extrafloral nectaries and on large, longer‐lived tree species.6. Given the nutrient‐poor nature of the Neotropics, host trees probably experience significant benefits from refuse fertilisation. Conversely,A. trigonabenefit from long‐term stable structural support for nests and access to nutrient‐rich extrafloral nectaries. Without clear costs to eitherA. trigonaor host trees, it is proposed that these positive interactions are preliminary evidence of a facultative mutualism.
Temperature response of permafrost soil carbon is attenuated by mineral protection
Authors: Gentsch Norman , Wild Birgit , Mikutta Robert , Čapek Petr , Diáková Katka , Schrumpf Marion , Turner Stephanie , Minnich Cynthia , Schaarschmidt Frank , Shibistova Olga , Schnecker Jörg , Urich Tim , Gittel Antje , Šantrůčková Hana , Bárta Jiři , Lashchinskiy Nikolay , Fuß Roland , Richter Andreas , Guggenberger Georg 
Published: May 2018

AbstractClimate change in Arctic ecosystems fosters permafrost thaw and makes massive amounts of ancient soil organic carbon (OC) available to microbial breakdown. However, fractions of the organic matter (OM) may be protected from rapid decomposition by their association with minerals. Little is known about the effects of mineral‐organic associations (MOA) on the microbial accessibility ofOMin permafrost soils and it is not clear which factors control its temperature sensitivity. In order to investigate if and how permafrost soilOCturnover is affected by mineral controls, the heavy fraction (HF) representing mostlyMOAwas obtained by density fractionation from 27 permafrost soil profiles of the Siberian Arctic. In parallel laboratory incubations, the unfractionated soils (bulk) and theirHFwere comparatively incubated for 175 days at 5 and 15°C. TheHFwas equivalent to 70 ± 9% of the bulkCO2respiration as compared to a share of 63 ± 1% of bulkOCthat was stored in theHF. Significant reduction ofOCmineralization was found in all treatments with increasingOCcontent of theHF(HF‐OC), clay‐size minerals and Fe or Al oxyhydroxides. Temperature sensitivity (Q10) decreased with increasing soil depth from 2.4 to 1.4 in the bulk soil and from 2.9 to 1.5 in theHF. A concurrent increase in the metal‐to‐HF‐OCratios with soil depth suggests a stronger bonding ofOMto minerals in the subsoil. There, the younger14C signature inCO2than that of theOCindicates a preferential decomposition of the more recentOMand the existence of aMOAfraction with limited access ofOMto decomposers. These results indicate strong mineral controls on the decomposability ofOMafter permafrost thaw and on its temperature sensitivity. Thus, we here provide evidence thatOMtemperature sensitivity can be attenuated byMOAin permafrost soils.
Release of TGF‐β1 into root canals with various final irrigants in regenerative endodontics: an in vitro analysis
Authors: Chae Y. , Yang M. , Kim J. 
Published: May 2018

AbstractAimTo investigate the release of growth factors into the root canal space after various final irrigants during regenerative endodontic procedures. The residual cytotoxic effect of final irrigants on stem cells from the apical papilla (SCAP) was also examined.MethodologyTo measure the release of TGF‐β1, root segments (8 mm long) were irrigated with 1.5% NaOCl followed by 20 mL of final irrigants; Saline, 17% EDTA, 10% citric acid, 10% or 37% phosphoric acid. Specimens were then immersed into culture medium for 24 h and the supernatants were collected to measure TGF‐β1 by ELISA. For the cytotoxicity of residual final irrigants, dentine chips (5 × 5 × 1 mm) treated with irrigants as above were placed in the upper chamber of transwell system. Stem cells from the apical papilla were incubated indirectly in the lower chamber for 24 h and MTS assay was performed after 24 h. The surfaces of irrigated root canals were examined for smear layer with a scanning electron microscope (SEM). Log transformation was performed for ELISA data to compare different groups (one‐way ANOVA, α = 0.05).ResultsTen percent citric acid released the greatest amount of TGF‐β1 amongst all groups, which was significantly different to 17% EDTA (P < 0.01). All dentine chips irrigated with the irrigants showed no significant difference of cytotoxicity on SCAP compared to nonirrigated dentine (P > 0.05). SEM revealed completely open dentinal tubules in 10% citric acid, whereas 17% EDTA was associated with partially open dentinal tubules.ConclusionsTen percent citric acid was effective as a final irrigant for releasing TGF‐β1 with good biocompatibility in regenerative endodontics.
Young adults' knowledge and attitudes towards cardiovascular disease: A systematic review and meta‐analysis
Authors: Trejo Ronald , Cross Wendy , Stephenson John , Edward Karen‐leigh 
Published: May 2018

Aims and objectivesTo explore young adults' knowledge and attitudes of cardiovascular disease and its risk factors.BackgroundCardiovascular disease morbidity is rising and mortality is declining among young adults. However, the knowledge of cardiovascular disease by young adults is not well known.DesignA systematic review with meta‐analysis was used.MethodsThe databases of CINHAL, MEDLINE Complete, PsycINFO and Psycarticles were searched for all studies published before June 2016. Search terms included cardiovascular disease, young adult, attitude and knowledge. Papers were included if they were published in English and reported quantitative research with a study population between the ages of 18–34 years, with a focus on knowledge and attitudes to cardiovascular disease. Meta‐analyses were conducted to assess the extent of knowledge of risk factors on heart disease.ResultsNine risk factors for cardiovascular disease were identified by the respondents; smoking (synthesised estimate of 55% of respondents identifying as a risk factor, 95% confidence interval of synthesised estimate 45%–65%); obesity (27%, 95% CI, 26%–29%); high blood cholesterol (33%, 95% CI, 12%–54%); high blood pressure (25%, 95% CI, 18%–32%); genetic factors (26%, 95% CI, 23%–29%); physical inactivity (39%, 95% CI, 30%–47%); stress (49%, 95% CI, 48%–51%); advancing age (10%, 95% CI, 8%–12%) and diet (55%, 95% CI, 54%–56%).ConclusionYoung adults demonstrate limited knowledge and poor attitudes regarding cardiovascular disease and its risk factors. The finding of this review demonstrates that there is an urgent need to build knowledge of cardiovascular risk identification in this population group.Relevance to clinical practiceIncreasing cardiovascular disease in young adults will put stress in the healthcare system financially and economically. There is a need of awareness of cardiovascular disease in this population group.
A broader understanding of care managers’ attitudes of advance care planning: A concurrent nested design
Authors: Aultman Julie , Baughman Kristin R , Ludwick Ruth 
Published: May 2018

Aims and ObjectivesTo examine barriers of advance care planning (ACP) experienced by care managers (CMs) through a mixed methods approach. A concurrent nested design was used to acquire a deeper understanding of ACP and to identify nuances between quantitative and qualitative data.BackgroundPast quantitative studies on providers have identified barriers related to time, culture, knowledge, responsibility and availability of legal documents. These barriers, and accompanying attitudes and feelings, have been taken at face value without rich qualitative data to identify under what conditions and to what extent a barrier impacts care.DesignA two‐part multisite, mixed methods study was conducted using surveys and focus groups.MethodsSurveys were completed by 458 CMs at 10 Area Agencies on Aging and 62 participated in one of eight focus groups. Data were analysed using a concurrent nested design with individual data analysis and a merged data approach.ResultsThere were three main distinctions between the quantitative and qualitative data. First, while CMs reported on the survey that ACP was not too time consuming, focus group data revealed that time was an issue especially related to competing priorities. Second on the survey 60% of the CMS reported they had enough knowledge, but qualitative data revealed about more nuances. Last, the reported comfort levels in the quantitative data were less overt in the qualitative date where additional feelings and attitudes were revealed, for example, frustration with families, preferences for more physician involvement.ConclusionsCare managers reported their attitudes about ACP, clarified through a rigorous mixed methods analysis. Care managers can successfully lead ACP discussions, but require further education, resources and team‐based guidance.Relevance to Clinical PracticeAdvance care planning is essential for reducing emotional, social and financial burdens associated with healthcare decision‐making, and CMs can positively impact ACP discussions when appropriately supported by the clinical community. The many nuances in the ACP process that we found illustrate the need for ongoing discussions, education and research on this important topic.
Matrix‐glycoprotein interactions required for budding of a plant nucleorhabdovirus and induction of inner nuclear membrane invagination
Authors: Sun Kai , Zhou Xin , Lin Wenye , Zhou Xueping , Jackson Andrew O. , Li Zhenghe 
Published: May 2018

SummaryNucleorhabdoviruses such as Sonchus yellow net virus (SYNV) replicate in the nuclei and undergo morphogenesis at the inner nuclear membrane (IM) in plant cells. Mature particles are presumed to form by budding of the Matrix (M) protein‐nucleocapsid complexes through host IMs to acquire host phospholipids and the surface glycoproteins (G). To address mechanisms underlying nucleorhabdovirus budding, we generated recombinant SYNV G mutants containing a truncated amino‐terminal (NT) or carboxyl‐terminal (CT) domain. Electron microscopy and sucrose gradient centrifugation analyses showed that the CT domain is essential for virion morphogenesis whereas the NT domain is also required for efficient budding. SYNV infection induces IM invaginations that are thought to provide membrane sites for virus budding. We found that in the context of viral infections, interactions of the M protein with the CT domain of the membrane‐anchored G protein mediate M protein translocation and IM invagination. Interestingly, tethering the M protein to endomembranes, either by co‐expression with a transmembrane G protein CT domain or by artificial fusion with the G protein membrane targeting sequence, induces IM invagination in uninfected cells. Further evidence to support functions of G‐M interactions in virus budding came from dominant negative effects on SYNV‐induced IM invagination and viral infections that were elicited by expression of a soluble version of the G protein CT domain. Based on these data, we propose that cooperative G‐M interactions promote efficient SYNV budding.
Priming patient safety: A middle‐range theory of safety goal priming via safety culture communication
Authors: Groves Patricia S. , Bunch Jacinda L. 
Published: May 2018

AbstractThe aim of this paper is discussion of a new middle‐range theory of patient safety goal priming via safety culture communication. Bedside nurses are key to safe care, but there is little theory about how organizations can influence nursing behavior through safety culture to improve patient safety outcomes. We theorize patient safety goal priming via safety culture communication may support organizations in this endeavor. According to this theory, hospital safety culture communication activates a previously held patient safety goal and increases the perceived value of actions nurses can take to achieve that goal. Nurses subsequently prioritize and are motivated to perform tasks and risk assessment related to achieving patient safety. These efforts continue until nurses mitigate or ameliorate identified risks and hazards during the patient care encounter. Critically, this process requires nurses to have a previously held safety goal associated with a repertoire of appropriate actions. This theory suggests undergraduate educators should foster an outcomes focus emphasizing the connections between nursing interventions and safety outcomes, hospitals should strategically structure patient safety primes into communicative activities, and organizations should support professional development including new skills and the latest evidence supporting nursing practice for patient safety.