bluuebunny/crossref_metadata_2025_split huggingface dataset:
Incidence of acute hepatitis A among HIV‐positive patients during an outbreak among MSM in Taiwan: Impact of HAV vaccination
Authors: Chen Guan‐Jhou , Lin Kuan‐Yin , Sun Hsin‐Yun , Sheng Wang‐Huei , Hsieh Szu‐Min , Huang Yi‐Chia , Cheng Aristine , Liu Wen‐Chun , Hung Chien‐Ching , Chang Shan‐Chwen 
Published: May 2017

AbstractBackgroundAn unprecedented outbreak of acute hepatitis A has occurred among MSM in Taiwan since June 2015. We aimed to describe the seroepidemiology of HAV infection and to investigate the relationship between HAV vaccination and the incidence of acute hepatitis A among HIV‐positive patients at the largest designated hospital for HIV care during the outbreak.MethodsBetween 2012 and 2016, the HAV serostatus, vaccination history and clinical characteristics of HIV‐positive patients were retrospectively reviewed. A case‐control study was performed to identify the factors associated with acute hepatitis A. The trends of HAV vaccination rate and incidence of acute hepatitis A among HAV‐seronegative patients were examined during the outbreak.ResultsDuring the 4.5‐year period, 2088 HIV‐positive patients with a mean age of 37.7 years and 90.2% being MSM were included. The overall HAV seroprevalence was 34.3%, which was significantly higher in older and non‐MSM patients. The estimated incidence rate of acute hepatitis A was 52.6 cases per 1000 person‐years of follow‐up during the outbreak. The associated factors with acquiring acute hepatitis A were recent syphilis and having not received HAV vaccines. The HAV vaccination rate during the outbreak increased from 4.7% to 70.6% and the incidence rate of acute hepatitis A declined when up to 65% of the patients were immunized or tested positive for HAV.ConclusionsThe seroprevalence of HAV infection was low in the younger HIV‐positive individuals. Prevention of acute hepatitis A was achieved among HIV‐positive, HAV‐seronegative patients through HAV vaccination and increased herd immunity during the ongoing outbreak.
High efficacy of Sofosbuvir plus Simeprevir in a large cohort of Spanish cirrhotic patients infected with genotypes 1 and 4
Authors: Mariño Zoe , Pascasio‐Acevedo Juan M. , Gallego Adolfo , Diago Moisés , Baliellas Carme , Morillas Rosa , Prieto Martín , Moreno José M. , Sánchez‐Antolín Gloria , Vergara Mercedes , Forné Montserrat , Fernández Inmaculada , Castro María A. , Pascual Sonia , Gómez Alexandra , Castells Lluis , Montero José L. , Crespo Javier , Calleja José L. , García‐Samaniego Javier , Carrión Jose A. , Arencibia Ana C. , Blasco Alejandro , López‐Núñez Carmen , Sánchez‐Ruano Juan J. , Gea‐Rodríguez Francisco , Giráldez Álvaro , Cabezas Joaquín , Hontangas Vanessa , Torras Xavier , Castellote Jose , Romero‐Gómez Manuel , Turnes Juan , de Artaza Tomás , Narváez Isidoro , Cuervas‐Mons Valentín , Forns Xavier 
Published: May 2017

AbstractBackground and AimsHepatitis C (HCV) therapy with Sofosbuvir (SOF)/Simeprevir (SMV) in clinical trials and real‐world clinical practice, showed high rates of sustained virological response (SVR) in non‐cirrhotic genotype (GT)‐1 and GT‐4 patients. These results were slightly lower in cirrhotic patients. We investigated real‐life effectiveness and safety of SOF/SMV with or without ribavirin (RBV) in a large cohort of cirrhotic patients.MethodsThis collaborative multicentre study included data from 968 patients with cirrhosis infected with HCV‐GT1 or 4, treated with SOF/SMV±RBV in 30 centres across Spain between January‐2014 and December‐2015. Demographic, clinical, virological and safety data were analysed.ResultsOverall SVR was 92.3%; the majority of patients were treated with RBV (62%) for 12 weeks (92.4%). No significant differences in SVR were observed between genotypes (GT1a:94.3%; GT1b:91.7%; GT4:91.1%). Those patients with more advanced liver disease (Child B/C, MELD≥10) or portal hypertension (platelet count≤100×109/L, transient elastography≥21 Kpa) showed significantly lower SVR rates (84.4%‐91.9%) than patients with less advanced liver disease (93.8%‐95.9%, P<.01 in all cases). In the multivariate analysis, the use of RBV, female gender, baseline albumin≥35 g/L, MELD<10 and lack of exposure to a triple therapy regimen were independent predictors of SVR (P<.05). Serious adverse events (SAEs) and SAE‐associated discontinuation events occurred in 5.9% and 2.6%.ConclusionsIn this large cohort of cirrhotic patients managed in the real‐world setting in Spain, SOF/SMV±RBV yielded to excellent SVR rates, especially in patients with compensated liver cirrhosis. In addition, this combination showed to be safe, with low rates of SAEs and early discontinuations.
Beyond Political Theology and its Liquidation: From Theopolitical Monotheism to Trinitarianism
Authors: Mrówczyński‐Van Allen Artur 
Published: May 2017

AbstractOne of the central theological challenges facing Erik Peterson was to help the mid‐twentieth century Catholic Church define its relationship with the wider world. He responded by advancing a distinctive understanding of the ‘polis.’ In this essay, I critically analyze Peterson's central and perhaps best known proposal about how the Church ought to negotiate the modern world — encapsulated in his expression, the ‘liquidation of political theology.’ I contend that Peterson's proposal is not congruent with a right understanding of patristic trinitarian monarchy, although a view that stands in sharp contrast to that of Carl Schmitt. Notwithstanding the effectiveness of Peterson's critique of Schmitt's political theology, I argue that Peterson nonetheless fails in his exposition of the thought of Gregory of Nazianzus and therefore in his interpretation of the role of the Church in what we have learned to call the ‘political’ and the ‘social.’ I conclude by outlining several ways that the Church today might take up the challenge of regaining a truly political thought, a new ekklesioteia, nourished by the monarchy of the triune God.
Sleep patterns in relation to dietary patterns and cardio‐metabolic risk: An update from Drummond Pump Priming Award recipients
Authors: Darzi J. , Al Khatib H. , Pot G. K. 
Published: May 2017

AbstractThis article provides an update on the project ‘Sleep patterns in relation to dietary patterns and cardio‐metabolic risk’, which received funding from the British Nutrition Foundation (BNF) Drummond Pump Priming Award. Studying the relationship between sleep, the biological clock, timing of eating and nutrition is part of a new research area termed chrono‐nutrition. With the help of the BNF award, a PhD project was set up to investigate the effects of sleep duration and quality on energy balance, dietary intake and quality, and cardio‐metabolic risk factors. The project included three studies: (1) a systematic review and meta‐analysis investigating whether partial sleep deprivation results in positive energy balance; (2) a cross‐sectional study exploring associations between energy balance, dietary intake and quality, chrono‐nutrition and cardio‐metabolic risk factors; and (3) a randomised controlled intervention feasibility study investigating whether sleep extension in participants with chronic mild sleep deprivation can improve energy balance, diet quality, body composition and cardio‐metabolic risk profile. The systematic review showed that partial sleep deprivation results in a net positive energy balance arising from a significantly higher energy intake of 385 kcal/day, with no compensatory effect on energy expenditure. Results from the cross‐sectional and randomised controlled feasibility studies are expected later this year. Overall, the project will help to establish whether sleep extension can be used in combination with existing weight management strategies to reduce the burden of obesity and metabolic dysregulation, which are major public health threats.
Sympathetic ANS modulation of pupil diameter in emotional scene perception: Effects of hedonic content, brightness, and contrast
Authors: Bradley Margaret M. , Sapigao Rosemarie G. , Lang Peter J. 
Published: May 2017

AbstractA series of studies investigated the effects of hedonic content, brightness, and contrast on pupil diameter during free viewing of natural scenes, assessing the amplitude of the initial light reflex and subsequent sustained pupil diameter change. Hedonic picture content varied from highly arousing scenes of erotica and violence to scenes depicting nature, babies, loss, contamination, food, and more. Despite equivalent overall picture brightness and contrast, pupil diameter still varied as a function of the local brightness of central vision at fixation. Statistical (Experiment 1) and methodological (Experiment 2, 3) solutions produced complementary data indicating that scenes of erotica and violence reliably attenuate the amplitude of the initial light reflex and prompt enhanced late diameter pupil changes, compared to other scene contents. A principal components analysis supported the hypothesis that a single sympathetically mediated process enhances pupil dilation during picture viewing, modulating both initial constriction and late diameter changes. Rather than being a subtle index of “liking,” pupil diameter is primarily sensitive to events that reliably elicit measurable sympathetic nervous system activity.
Integrative taxonomy improves understanding of native beneficial fauna: revision of the Nearctic Peristenus pallipes complex (Hymenoptera: Braconidae) and implications for release of exotic biocontrol agents
Authors: ZHANG Y. MILES , RIDENBAUGH RYAN D. , SHARANOWSKI BARBARA J. 
Published: May 2017

AbstractThe Nearctic Peristenus pallipes complex (Hymenoptera: Braconidae) consists of two species groups that are further divided into nine species, separated largely using ecological rather than morphological differences. The species are re‐examined with an integrative approach using morphometric multivariate ratios, molecular (COI and CytB), and ecological data to test the validity of the nine species. The data support only three valid species [P. dayi Goulet, P. mellipes (Cresson) and P. howardi Shaw] rather than nine. New synonymies include: P. braunae Goulet under P. dayi Goulet 2006 syn.n.; P. carcamoi Goulet, P. otaniae Goulet and P. pseudopallipes (Loan) under P. mellipes (Cresson) syn.n., and finally P. broadbenti Goulet 2006 and P. gillespiei Goulet 2006 under P. howardi Shaw 1999 syn.n. In light of these taxonomic revisions, the biology and distributions of the Nearctic P. pallipes complex are updated, resulting in three morphologically variable, widespread, multivoltine species rather than nine largely univoltine species with patchy distributions. The integrative taxonomic approach used here allowed for a more accurate delineation of native fauna and their potential to be competitively displaced by foreign biocontrol agents.
Treatment of ibuprofen intoxication in a dog via therapeutic plasma exchange
Authors: Walton Stuart , Ryan Kirk A. , Davis Jennifer L. , Acierno Mark 
Published: May 2017

AbstractObjectiveTo describe the treatment of ibuprofen intoxication with therapeutic plasma exchange in a dog (TPE).SummaryA 13‐year‐old male neutered mixed breed dog presented after ingesting approximately 200 mg/kg of ibuprofen. Treatment consisted of supportive medical therapy with IV fluids, gastrointestinal protectants, antiemetics and prostaglandin analogs, and TPE. A cycle of TPE was performed over 180 minutes, achieving 1.5 plasma volume exchanges. During therapy, heparinized blood and effluent samples were collected. Ibuprofen concentrations were determined in the samples by high‐pressure liquid chromatography. Post TPE, the dog was continued on supportive medical therapy and was discharged 96 hours after the overdose.New or Unique InformationThis report describes the use of TPE as an adjunct for ibuprofen intoxication. An 85% reduction in plasma ibuprofen concentration occurred and recovery from a potentially lethal ingestion of ibuprofen was achieved with TPE and supportive care. TPE should be considered when presented with acute ibuprofen intoxication due to the rapid and efficacious nature of therapy.
Principles for Measurability in Protocol Design
Authors: Allman Mark , Beverly Robert , Trammell Brian 
Published: May 2017

Measurement has become fundamental to the operation of networks and at-scale services---whether for management, security, diagnostics, optimization, or simply enhancing our collective understanding of the Internet as a complex system. Further, measurements are useful across points of view---from end hosts to enterprise networks and data centers to the wide area Internet. We observe that many measurements are decoupled from the protocols and applications they are designed to illuminate. Worse, current measurement practice often involves the exploitation of side-effects and unintended features of the network; or, in other words, the artful piling of hacks atop one another. This state of affairs is a direct result of the relative paucity of diagnostic and measurement capabilities built into today's network stack.
Given our modern dependence on ubiquitous measurement, we propose \emph{measurability} as an explicit low-level goal of current protocol design, and argue that measurements should be available to all network protocols throughout the stack. We seek to generalize the idea of measurement \emph{within} protocols, e.g., the way in which TCP relies on measurement to drive its end-to-end behavior. Rhetorically, we pose the question: \textit{what if the stack had been built with measurability and diagnostic support in mind?} We start from a set of principles for explicit measurability, and define primitives that, were they supported by the stack, would not only provide a solid foundation for protocol design going forward, but also reduce the cost and increase the accuracy of measuring the network.
Abstract A15: Epigenetic up-regulation of ribosome biogenesis and more aggressive phenotype triggered by the lack of the histone demethylase JHDM1B in mammary epithelial cells
Authors: Galbiati Alice , Penzo Marianna , Bacalini Maria Giulia , Onofrillo Carmine , Guerrieri Ania Naila , Garagnani Paolo , Franceschi Claudio , Treré Davide , Montanaro Lorenzo 
Published: May 2017

Abstract
Alterations of ribosome biogenesis and protein synthesis play a direct role in the development and the behavior of tumors. The accessibility and transcription of ribosomal genes are controlled at several levels, with their epigenetic regulation being one of the most important. Here we explored the JmjC domain-containing histone demethylase 1B (JHDM1B) function in the epigenetic control of rDNA transcription. Since JHDM1B is a negative regulator of gene transcription, we focused on the effects induced by its downregulation. We studied the consequences of inducible JHDM1B knock-down (KD) in cell lines derived from transformed (MDA-MB-231) and untransformed (MCF-10A) mammary epithelial cells. In these cellular models, sustained JHDM1B down-regulation triggered an increase in 45S pre-rRNA transcription and processing, associated with a re-modulation of the H3K36me2 levels at the rDNA loci. By means of the EpiTYPER assay, we observed that JHDM1B KD reproducibly induced quantitative changes in DNA methylation of specific CpG sites in rDNA genes. By polysomal profile analysis, we also found that JHDM1B KD induced an higher content of ribosomes in both the pre-polysomal and polysomal fractions indicating an increase in global protein synthesis. We then investigated in vitro and in vivo the behavior of cells after JHDM1B KD and the associated stimulation of ribosomes biogenesis. JHDM1B down-regulation conferred more aggressive features to the tested cellular models, which acquired a greater clonogenic and invasive potential in vitro. The study of tumors generated in nude Balb/c mice after xenografting MDA-MB-231 cells, indicated that JHDM1B KD triggered an incremental (although not statistically significant) trend in tumor growth. In addition, the selective nucleolar staining of sections from these tumors revealed a significant increase in the average nucleolar area after JHDM1B KD. Taken together, these data indicate that the reduction of JHDM1B leads to an increase in ribosome production and to a more aggressive cellular behavior in mammary gland cells.
Citation Format: Alice Galbiati, Marianna Penzo, Maria Giulia Bacalini, Carmine Onofrillo, Ania Naila Guerrieri, Paolo Garagnani, Claudio Franceschi, Davide Treré, Lorenzo Montanaro. Epigenetic up-regulation of ribosome biogenesis and more aggressive phenotype triggered by the lack of the histone demethylase JHDM1B in mammary epithelial cells. [abstract]. In: Proceedings of the AACR Special Conference on Translational Control of Cancer: A New Frontier in Cancer Biology and Therapy; 2016 Oct 27-30; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2017;77(6 Suppl):Abstract nr A15.
Abstract A17: Probing a translational switch involved in tumor angiogenesis
Authors: Ramachandran Maya , Mitra Somdeb , Gonzalez Ruben L. 
Published: May 2017

Abstract
As a tumor proliferates, it rapidly outgrows its blood supply, creating an oxygen-starved environment. Low oxygenation (hypoxia) suppresses the canonical biochemical pathway through which the translation of messenger RNAs (mRNAs) into proteins by the ribosome is typically initiated. Despite shutting down this general mechanism for initiating protein synthesis, the tumor can continue to initiate translation of a subset of mRNAs that are involved in angiogenesis and tumor survival. To explain this observation, it has been proposed that, in addition to the eukaryotic mRNA-specific 7-methyl guanosine cap at the 5' end, these pro-angiogenic mRNAs, of which Fibroblast Growth Factor-9 (FGF9) and Hypoxia Inducible Factor 1α (HIF1α) are prototypical members, contain highly stable structures in their 5' untranslated regions. These structures, also referred to as Cap Independent Translation Enhancers (CITEs), form part of a switch that activates a non-canonical pathway for initiating translation, presumably by binding directly to eukaryotic initiation factor 4G (eIF4G), thereby recruiting ribosomes in a manner distinct from the canonical 5' cap-dependent mechanism. To test this hypothesis, here we report the binding affinities of pro-angiogenic mRNAs, as well as control mRNAs lacking CITEs, to eIF4G as a measure of their ability to initiate translation in the hypoxic environment of a tumor. Understanding the dynamics of eIF4G-CITE interactions can inform the design and development of novel angiogenesis inhibitors that function by targeting these interactions.
Citation Format: Maya Ramachandran, Somdeb Mitra, Ruben L. Gonzalez, Jr. Probing a translational switch involved in tumor angiogenesis. [abstract]. In: Proceedings of the AACR Special Conference on Translational Control of Cancer: A New Frontier in Cancer Biology and Therapy; 2016 Oct 27-30; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2017;77(6 Suppl):Abstract nr A17.
Abstract A20: Baseline IL-17 receptor signaling is essential for controlling aberrant JNK-dependent cellular proliferation via maintenance of endogenous level of ubiquitin-editing enzyme A20
Authors: Yan Chi , Lei Yang , Greenshields Anna L. , Hoskin David W. , Lin Tong-Jun , Wang Jun 
Published: May 2017

Abstract
The molecular mechanisms underlying aberrant activation of NF-κB and JNK in cancer remain incompletely understood. Here, we demonstrate that baseline IL-17 receptor (IL-17R) signaling is essential for controlling aberrant NF-κB and JNK activation, and restraining JNK-dependent homeostatic cellular proliferation. Using a shRNA knockdown approach, we demonstrated in two murine tumor cell lines that IL-17RA silencing markedly enhanced tumor cell growth in vitro and in vivo. Through mapping IL-17R signaling pathways, we further demonstrated that baseline IL-17A/IL-17R signaling actively restrained JNK phosphorylation in vitro and in vivo via maintenance of basal expression of the ubiquitin-editing enzyme A20, a negative regulator of NF-κB and JNK. Remarkably, IL-17RA reconstitution evidently restored the A20 level, and suppressed cell proliferation and JNK activity in tumor cells. The reconstitution of A20 in IL-17RA knockdown subclones is able to restore the normal rate of cellular proliferation and associated JNK/c-Jun activity. Finally, meta-analysis of human cancer microarray and RNA sequencing datasets confirmed close co-expression of IL-17RA and A20. Furthermore, alterations (mutation, upregulation or downregulation) of IL-17RA level in melanoma and ER+ breast cancer patients showed poor survival rate compared to the respective patients with normal baseline IL-17RA expression. Together, our data demonstrates a previously unrecognized molecular mechanism underlying aberrant activation of NF-κB and JNK in cancer cells. This work has significantly advanced our understanding of the biological role of the proinflammatory IL-17R signaling and highlights its unique role in the maintenance of A20 to regulate the pathogenesis of human cancer at translational level.
Citation Format: Chi Yan, Yang Lei, Anna L. Greenshields, David W. Hoskin, Tong-Jun Lin, Jun Wang. Baseline IL-17 receptor signaling is essential for controlling aberrant JNK-dependent cellular proliferation via maintenance of endogenous level of ubiquitin-editing enzyme A20. [abstract]. In: Proceedings of the AACR Special Conference on Translational Control of Cancer: A New Frontier in Cancer Biology and Therapy; 2016 Oct 27-30; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2017;77(6 Suppl):Abstract nr A20.
Abstract A22: Hypoxia-mediated translational control of hypoxia inducible factor 1 alpha through aldolase A feedback regulation in lung carcinogenesis
Authors: Chang Yu-Chan , Hsiao Michael 
Published: May 2017

Abstract
Lung cancer cells grow in-situ during low-oxygen situation and usually results in invasion and is frequently recurrent after therapy. However, the oxygen-mediated translation control of the metabolic events in lung cancer remains largely unknown. By using the integrated transcriptomics data and the shRNA library against glycolytic enzymes, here we identified that Aldolase A (ALDOA) up-regulation is highly correlated with migratory/invasive activity of lung cancer cells and poorer clinical outcomes. Significantly, knockdown of Aldolase A inhibited in vitro and in vivo migratory/invasive activity of lung cancer cell line with high ALDOA expression. Complementary, enforced overexpression of exogenous ALDOA promoted migration/invasion. Furthermore, microarray and Ingenuity pathway analyses reveal that ALDOA-driven lung cancer metastasis likely recruits Hypoxia-inducible factor 1 alpha (HIF1α)-associated signaling pathway. There were no significance changes at the mRNA level of HIF1α in ALDOA two-way models. However, HIF1α protein was found stabilized in hypoxic or normoxic condition through ALDOA overexpression to decrease prolyl hydroxylase (PHD) activity for hydroxylation-form of HIF1α to activate downstream genes including CXCR4, MMP9 in lung carcinogenesis. Interesting, HIF1α also was found to bind hypoxia-response element (HRE) domain of ALDOA to activate its transcription and form a positive feedback loop. IHC staining results further demonstrate that Aldolase A and HIF1α expression is positively correlated in clinical lung cancer tissues and the signature of high-level Aldolase A and HIF1α; expression strongly associates with worst survival probability in lung cancer patients. Our results not only unveil molecular mechanism by which Aldolase A promotes lung cancer metastasis via inducing the HIF1α activity but also provide a novel therapeutic strategy to combat malignant lung cancer via targeting ALDOA.
Citation Format: Yu-Chan Chang, Michael Hsiao. Hypoxia-mediated translational control of hypoxia inducible factor 1 alpha through aldolase A feedback regulation in lung carcinogenesis. [abstract]. In: Proceedings of the AACR Special Conference on Translational Control of Cancer: A New Frontier in Cancer Biology and Therapy; 2016 Oct 27-30; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2017;77(6 Suppl):Abstract nr A22.