bluuebunny/crossref_metadata_2025_split huggingface dataset:
Fulminant cardiac sarcoidosis resembling giant cell myocarditis: a case report
Authors: Jiang Ginger Y , Cai Qizhe , Grandin E Wilson , Sabe Marwa A 
Published: March 2021

Abstract

Background
Severe cardiac sarcoidosis (CS) can share clinical and histopathologic features with giant cell myocarditis (GCM).

Case summary
A 56-year-old female presented with 1 week of exertional chest pressure and dyspnoea. Echocardiogram demonstrated extensive regional dysfunction with left ventricular ejection fraction (LVEF) 38%. Cardiac catheterization revealed no obstructive coronary artery disease and cardiac index 1.5 L/min/m2. Cardiac magnetic resonance imaging (MRI) demonstrated diffuse late gadolinium enhancement. Positron emission tomography with fluorodeoxyglucose (FDG) (FDG-PET) computed tomography showed FDG uptake in the anteroseptal and anterior wall and no extracardiac activity. Endomyocardial biopsy (EMB) demonstrated fragments of endocardial fibrosis with mixed inflammatory infiltrate including histiocytic giant cells, which could be due to CS or GCM. She was initially treated for GCM with high dose steroids, tacrolimus, and mycophenolate mofetil. Repeat EMB was pursued and demonstrated multiple granulomas with sharp demarcation from adjacent uninvolved myocardium consistent with CS. A dual-chamber implantable cardioverter-defibrillator was placed, and immunosuppression was changed to prednisone alone with plan for infliximab.

Discussion
This case illustrates a rare presentation of fulminant isolated CS. Endomyocardial biopsy with sufficient tissue was critical to establish a diagnosis and initiate appropriate immunosuppression.
Immunoglobulin G4-related masses surrounding coronary arteries: a case report
Authors: Nakamura Takuya , Goryo Yutaka , Isojima Takuya , Kawata Hiroyuki 
Published: March 2021

Abstract

Background
Immunoglobulin G4 (IgG4)-related disease (IgG4-RD) is an immune-mediated fibroinflammatory condition with high serum IgG4 levels affecting various organs, such as the pancreas, lacrimal and salivary glands, thyroid, kidney, and lung. Typical cardiovascular manifestations of IgG4-RD include periaortitis, coronary arteritis, and pericarditis. However, reports of IgG4-RD associated with coronary arteritis are rare. Here, we report a case of IgG4-related masses surrounding the coronary arteries.

Case summary
A 59-year-old man was referred to our hospital because of mediastinal masses detected by computed tomography (CT). Coronary CT angiography revealed masses surrounding the right coronary artery and the left anterior descending coronary artery. An elevated serum level of IgG4 and histological findings led to the diagnosis of IgG4-related coronary arteritis with mass formation. Coronary angiography showed numerous feeding arteries to the masses, which were demonstrated as multiple microchannels in the intravascular ultrasound (IVUS) images.

Discussion
IgG4-RD involving the cardiovascular system has been reported. However, coronary artery disease associated with IgG4-RD is very rare, and the mechanism of mass formation in IgG4-related coronary arteritis is unclear. In our case, within the cardiovascular system, IgG4-RD was limited to the coronary arteries, suggesting that the affected coronary arteries may provide the necessary blood supply to the mass, thus, aiding its growth. These findings were supported by the images from coronary angiography and IVUS.
Concept of myocardial fatigue in reversible severe left ventricular systolic dysfunction from afterload mismatch: a case series
Authors: Tran Patrick , Joshi Mithilesh , Banerjee Prithwish 
Published: March 2021

Abstract

Background
There is already extensive literature on the natural history of hypertensive heart disease (HHD) and aortic stenosis (AS). Once these patients develop severe left ventricular systolic dysfunction (LVSD) despite guideline-directed therapy for heart failure (HF), it is often thought to be end-stage from irreversible adverse remodelling. Our case series challenges this traditional paradigm. A more holistic model that factors in the interactions between the ventricle and vasculature is required. Based on a novel hypothetical concept of myocardial fatigue, we propose that occasionally LVSD is not an inherent myocardial or valvular disease but a consequence of an arterial afterload mismatch. By addressing this, the ventricle may recover and contract efficiently in unison with the arterial system.

Case summary
We present two cases of severe LVSD in a young lady with long-standing essential hypertension and a gentleman with stable severe AS. Both patients were already established on HF medications. After optimizing their blood pressure control, repeat echocardiography revealed normalization of left ventricular ejection fraction within 3 months, along with a demonstrable improvement in ventricular–arterial coupling and for AS, a reduction in valvular-arterial impedance.

Discussion
Just as Frank–Starling’s law was discovered by initially drawing analogies to skeletal muscle behaviour, it is biologically plausible that cardiac fatigue can occur in the setting of afterload mismatch. The chance of recovery rests upon early recognition before it transitions to irreversible myocardial damage. Only by testing new emerging theories of HF can we galvanize original research and find new avenues to understanding this complex syndrome.
Patient-reported outcomes in symptom-driven remote arrhythmia monitoring: evaluation of the Dutch HartWacht-telemonitoring programme
Authors: Kolk Maarten Z H , Blok Sebastiaan , De Wildt Maud C C , Tjong Fleur V Y , Winter Michiel M , Tulevski Igor I , van den Born Bert-Jan H , Somsen G Aernout 
Published: March 2021

AbstractAimsThere is limited quantitative evidence on the effect of symptom-driven telemonitoring for cardiac arrhythmias on patient-reported outcomes. We evaluated the effect of a symptom-driven remote arrhythmia monitoring programme on the patient-reported health-related quality of life (HRQoL), sense of safety, physical limitations, and self-management.Methods and resultsThis was an observational retrospective longitudinal study of the symptom-driven HartWacht-telemonitoring programme using a remote single-lead electrocardiogram monitoring system. Real-world patient data from participants who were enrolled in the telemonitoring programme for (suspected) symptomatic atrial fibrillation (AF) between July 2017 and September 2019 were evaluated. Primary outcomes were the patient-reported generic HRQoL, disease-specific HRQoL, sense of safety, physical limitations, and self-management at date of enrolment, 3 months and 6 months of follow-up. Outcomes were compared to a historical control group consisting of AF patients receiving standard care. A total of 109 participants in the HartWacht programme [59 men (54%); mean age 61 ± 11 years; 72% diagnosed AF] were included in complete case analysis. There was no significant change in HRQoL and sense of safety during follow-up. A significant improvement in the perceived physical limitations was observed. The level of self-management declined significantly during follow-up. Comparisons to the historic control group (n = 83) showed no difference between the patient-reported disease-specific HRQoL, sense of safety and physical limitations at 6 months of follow-up.ConclusionSymptom-driven remote arrhythmia monitoring for AF does not seem to affect HRQoL and sense of safety, whereas the perceived physical limitations tend to improve. Patient-reported self-management declined during the first 6 months of participation.
LI Detector: a framework for sensitive colony-based screens regardless of the distribution of fitness effects
Authors: Parikh Saurin Bipin , Castilho Coelho Nelson , Carvunis Anne-Ruxandra 
Published: March 2021

AbstractMicrobial growth characteristics have long been used to investigate fundamental questions of biology. Colony-based high-throughput screens enable parallel fitness estimation of thousands of individual strains using colony growth as a proxy for fitness. However, fitness estimation is complicated by spatial biases affecting colony growth, including uneven nutrient distribution, agar surface irregularities, and batch effects. Analytical methods that have been developed to correct for these spatial biases rely on the following assumptions: (1) that fitness effects are normally distributed, and (2) that most genetic perturbations lead to minor changes in fitness. Although reasonable for many applications, these assumptions are not always warranted and can limit the ability to detect small fitness effects. Beneficial fitness effects, in particular, are notoriously difficult to detect under these assumptions. Here, we developed the linear interpolation-based detector (LI Detector) framework to enable sensitive colony-based screening without making prior assumptions about the underlying distribution of fitness effects. The LI Detector uses a grid of reference colonies to assign a relative fitness value to every colony on the plate. We show that the LI Detector is effective in correcting for spatial biases and equally sensitive toward increase and decrease in fitness. LI Detector offers a tunable system that allows the user to identify small fitness effects with unprecedented sensitivity and specificity. LI Detector can be utilized to develop and refine gene–gene and gene–environment interaction networks of colony-forming organisms, including yeast, by increasing the range of fitness effects that can be reliably detected.
Chemosensory signal transduction inCaenorhabditis elegans
Authors: Ferkey Denise M , Sengupta Piali , L’Etoile Noelle D 
Published: March 2021

AbstractChemosensory neurons translate perception of external chemical cues, including odorants, tastants, and pheromones, into information that drives attraction or avoidance motor programs. In the laboratory, robust behavioral assays, coupled with powerful genetic, molecular and optical tools, have made Caenorhabditis elegans an ideal experimental system in which to dissect the contributions of individual genes and neurons to ethologically relevant chemosensory behaviors. Here, we review current knowledge of the neurons, signal transduction molecules and regulatory mechanisms that underlie the response of C. elegans to chemicals, including pheromones. The majority of identified molecules and pathways share remarkable homology with sensory mechanisms in other organisms. With the development of new tools and technologies, we anticipate that continued study of chemosensory signal transduction and processing in C. elegans will yield additional new insights into the mechanisms by which this animal is able to detect and discriminate among thousands of chemical cues with a limited sensory neuron repertoire.
Dri1 mediates heterochromatin assembly via RNAi and histone deacetylation
Authors: Ban Hyoju , Sun Wenqi , Chen Yu-hang , Chen Yong , Li Fei 
Published: March 2021

Abstract
Heterochromatin, a transcriptionally silenced chromatin domain, is important for genome stability and gene expression. Histone 3 lysine 9 methylation (H3K9me) and histone hypoacetylation are conserved epigenetic hallmarks of heterochromatin. In fission yeast, RNA interference (RNAi) plays a key role in H3K9 methylation and heterochromatin silencing. However, how RNAi machinery and histone deacetylases (HDACs) are coordinated to ensure proper heterochromatin assembly is still unclear. Previously, we showed that Dpb4, a conserved DNA polymerase epsilon subunit, plays a key role in the recruitment of HDACs to heterochromatin during S phase. Here, we identified a novel RNA-binding protein Dri1 that interacts with Dpb4. GFP-tagged Dri1 forms distinct foci mostly in the nucleus, showing a high degree of colocalization with Swi6/Heterochromatin Protein 1. Deletion of dri1+ leads to defects in silencing, H3K9me, and heterochromatic siRNA generation. We also showed that Dri1 physically associates with heterochromatic transcripts, and is required for the recruitment of the RNA-induced transcriptional silencing (RITS) complex via interacting with the complex. Furthermore, loss of Dri1 decreases the association of the Sir2 HDAC with heterochromatin. We further demonstrated that the C-terminus of Dri1 that includes an intrinsically disordered (IDR) region and three zinc fingers is crucial for its role in silencing. Together, our evidences suggest that Dri1 facilitates heterochromatin assembly via the RNAi pathway and HDAC.
Anthropometric Variables as Mediators of the Association of Changes in Diet and Physical Activity With Inflammatory Profile
Authors: Cárdenas-Fuentes Gabriela , Lassale Camille , Martínez-González Miguel Ángel , Grau María , Salas-Salvadó Jordi , Corella Dolores , Serra-Majem Lluis , Warnberg Julia , Konieczna Jadwiga , Estruch Ramón , Pintó Xavier , Martínez J Alfredo , Vázquez Clotilde , Vidal Josep , Tur Josep A , Díaz-López Andrés , Lancova Hana , Fito Montserrat , Schröder Helmut 
Published: March 2021

AbstractBackgroundMechanisms underlying the associations of high levels of physical activity (PA) and adherence to the Mediterranean diet (MedDiet) with a better inflammatory profile remain unclear. Our objective was to assess the mediating role of changes in body mass index (BMI) and waist circumference (WC), as markers of body fat in the association of changes in PA and adherence to the MedDiet, with changes in the inflammatory profile.MethodThis study included 489 adults, aged 55–75 years, from the PREDIMED-Plus multicenter lifestyle intervention trial. An inflammatory score was calculated, based on 8 blood biomarkers: high-sensitivity C-reactive protein, interleukin 6, interleukin 8, interleukin 18, monocyte chemo-attractant protein-1, C-peptide, leptin, and regulated on activation, normal T-cell–expressed and secreted chemokine. Biomarkers, levels of PA, score of MedDiet adherence, BMI, and WC were measured at baseline and at 1-year follow-up. Linear regression models were fitted according to the Baron and Kenny framework for mediation analysis.ResultsChanges in BMI and WC mediated the association of both changes in PA and changes in the MedDiet adherence with the inflammatory score. Body mass index mediated 26% of the association of changes in total PA with the inflammatory profile, and 27% of the association of changes in the MedDiet, while WC mediated 13% and 12% of these associations, respectively.ConclusionIn older adults at high cardiovascular risk, increasing PA levels and adherence to a MedDiet during 1 year were associated with a lower inflammatory score, which was partly mediated by a reduction in body fat.Clinical Trials Registration NumberInternational Standard Randomized Controlled Trial Number: ISRCTN89898870; registration date July 24, 2014, retrospectively registered.
Reduced Physical Activity Alters the Leucine-Stimulated Translatome in Aged Skeletal Muscle
Authors: Mahmassani Ziad S , McKenzie Alec I , Petrocelli Jonathan J , de Hart Naomi M , Fix Dennis K , Kelly Joshua J , Baird Lisa M , Howard Michael T , Drummond Micah J 
Published: March 2021

AbstractPeriods of inactivity experienced by older adults induce nutrient anabolic resistance creating a cascade of skeletal muscle transcriptional and translational aberrations contributing to muscle dysfunction. The purpose of this study was to identify how inactivity alters leucine-stimulated translation of molecules and pathways within the skeletal muscle of older adults. We performed ribosomal profiling alongside RNA sequencing from skeletal muscle biopsies taken from older adults (n = 8; ~72 years; 6 F/2 M) in response to a leucine bolus before (Active) and after (Reduced Activity) 2 weeks of reduced physical activity. At both visits, muscle biopsies were taken at baseline, 60 minutes (early response), and 180 minutes (late response) after leucine ingestion. Previously identified inactivity-related gene transcription changes (PFKFB3, GADD45A, NMRK2) were heightened by leucine with corresponding changes in translation. In contrast, leucine also stimulated translational efficiency of several transcripts in a manner not explained by corresponding changes in mRNA abundance (“uncoupled translation”). Inactivity eliminated this uncoupled translational response for several transcripts, and reduced the translation of most mRNAs encoding for ribosomal proteins. Ingenuity Pathway Analysis identified discordant circadian translation and transcription as a result of inactivity such as translation changes to PER2 and PER3 despite unchanged transcription. We demonstrate inactivity alters leucine-stimulated “uncoupled translation” of ribosomal proteins and circadian regulators otherwise not detectable by traditional RNA sequencing. Innovative techniques such as ribosomal profiling continues to further our understanding of how physical activity mediates translational regulation, and will set a path toward therapies that can restore optimal protein synthesis on the transcript-specific level to combat negative consequences of inactivity on aging muscle.
Eikonal equation-basedP-wave seismic azimuthal anisotropy tomography of the crustal structure beneath northern California
Authors: Liu Yongsheng , Tong Ping 
Published: March 2021

SUMMARYDelineating spatial variations of seismic anisotropy in the crust is of great importance for the understanding of structural heterogeneities, regional stress regime and ongoing crustal dynamics. In this study, we present a 3-D anisotropic P-wave velocity model of the crust beneath northern California by using the eikonal equation-based seismic azimuthal anisotropy tomography method. The velocity heterogeneities under different geological units are well resolved. The thickness of the low-velocity sediment at the Great Valley Sequence is estimated to be about 10 km. The high-velocity anomaly underlying Great Valley probably indicates the existence of ophiolite bodies. Strong velocity contrasts are revealed across the Hayward Fault (2–9 km) and San Andreas Fault (2–12 km). In the upper crust (2–9 km), the fast velocity directions (FVDs) are generally fault-parallel in the northern Coast Range, which may be caused by geological structure; while the FVDs are mainly NE–SW in Great Valley and the northern Sierra Nevada possibly due to the regional maximum horizontal compressive stress. In contrast, seismic anisotropy in the mid-lower crust (12–22 km) may be attributed to the alignment of mica schists. The anisotropy contrast across the San Andreas Fault may imply different mechanisms of crustal deformation on the two sides of the fault. Both the strong velocity contrasts and the high angle (∼45° or above) between the FVDs and the strikes of faults suggest that the faults are mechanically weak in the San Francisco bay area (2–6 km). This study suggests that the eikonal equation-based seismic azimuthal anisotropy tomography is a valuable tool to investigate crustal heterogeneities and tectonic deformation.
New directions for leader personality research: breaking bad in foreign policy
Authors: Kaarbo Juliet 
Published: March 2021

Abstract
This article considers how leaders' personality traits change over time. I focus on how leaders become more authoritarian, overconfident and more mistake-prone; how, when and why do leaders ‘break bad’? Temporal evolution of leaders is an important topic given the long tenure of many political leaders and the influence these leaders have over policies, including foreign policies. There is very little work on how leaders' personalities develop and how they interact with changing constraints and opportunities. This article is an agenda-setting review, designed to push foreign policy analysis in new directions. This is especially important given the resurgence in research on personalities and the renewed interest in leaders. Drawing on diverse and multi-disciplinary scholarship on the psychological effects of aging, experience, learning and power-holding, this article develops expectations about leader personality change. I discuss challenges for research in this area, focusing on how ‘bad’ can be conceptualized, and offer specific avenues for future investigations.
Populism, nationalism and revisionist foreign policy
Authors: Jenne Erin K 
Published: March 2021

Abstract
Over the past decade, we have seen the rise of populist nationalist heads of state across a number of important electoral democracies—all of whom have made some version of the promise to make their countries ‘great again’. However, scholars are divided over whether these leaders' sometimes bombastic rhetoric has consistent or predictable effects on state foreign policy. This article introduces a framework for mapping the effects of populism and nationalism in foreign policy. In doing so, it draws on Essex School discourse analysis and sociological frame analysis to argue that representational crises at the sub-state level increase the popular resonance of ‘sovereigntist frames’ that diagnose the causes of perceived gaps in representation of the ‘authentic’ sovereign community at the international level and enjoin chief executives to resolve these gaps through revisionist foreign policy practices. The ethno-nationalist master frame prescribes policies and practices of lateral revisionism (conflict with neighbours or rival states), the populist frame prescribes systemic revisionism (conflict with allies and the international ‘establishment’), while the ethno-populist frame prescribes omni-revisionism (conflict with both). The article illustrates the effects of these disparate sovereigntist movements across three paired case-studies drawn from Europe, Latin America and the United States. It concludes that nationalism has greater destructive effects for the international system when combined with populism, demonstrating the importance of distinguishing nationalism and populism conceptually in order to isolate their separate and combined effects on foreign policy.
Targeting Immune Cell Metabolism in the Treatment of Inflammatory Bowel Disease
Authors: Zaiatz Bittencourt Vanessa , Jones Fiona , Doherty Glen , Ryan Elizabeth J 
Published: March 2021

Abstract
The cells of the immune system are highly dynamic, constantly sensing and adapting to changes in their surroundings. Complex metabolic pathways govern leukocytes’ ability to fine-tune their responses to external threats. Mammalian target of rapamycin complex 1 and hypoxia inducible factor are important hubs of these pathways and play a critical role coordinating cell activation and proliferation and cytokine production. For this reason, these molecules are attractive therapeutic targets in inflammatory disease. Insight into perturbations in immune cell metabolic pathways and their impact on inflammatory bowel disease (IBD) progression are starting to emerge. However, it remains to be determined whether the aberrations in immune metabolism that occur in gut resident immune cells contribute to disease pathogenesis or are reflected in the peripheral blood of patients with IBD. In this review, we explore what is known about the metabolic profile of T cells, monocytes, macrophages, dendritic cells, and natural killer cells in IBD and discuss the potential of manipulating immune cell metabolism as a novel approach to treating IBD.