bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of nearby piles and soil properties on thermal behaviour of a field-scale energy pile
Authors: Moradshahi Aria , Faizal Mohammed , Bouazza Abdelmalek , McCartney John S. 
Published: October 2020

The thermal response of an energy field scale pile that is part of a pair of energy piles spaced at a centre-to-centre distance of 3.5 m (i.e., 6D, where D is the pile diameter), was examined experimentally and numerically. Three field tests were conducted to assess the axial and radial thermal responses of the energy pile: (i) heating of the energy pile alone, (ii) heating of both energy piles simultaneously, and (iii) heating of the other energy pile while the considered energy pile was not heated. Good agreement was obtained between the experimental and numerical evaluations of the energy pile during the tests. A parametric study of the validated numerical model was performed for each of the three tests to understand the effects of varying soil thermal conductivity, thermal expansion coefficient, and elastic modulus on the thermal response of the considered energy pile. The numerical results confirmed the field results that radial thermal stresses in the energy piles were insignificant compared to axial thermal stresses. The impact of elastic modulus of the soil was more significant on the thermal stresses of the energy pile compared to the effects of soil thermal conductivity and thermal expansion coefficient. The thermal stresses of the considered energy pile were not significantly affected when both energy piles were heated simultaneously, even though ground temperature changes between the energy piles were more significant due to thermal interaction. Only minor thermal effects on the non-thermal pile were observed during heating of one of the energy piles for different soil properties.
A note on the total action of 4D Gauss–Bonnet theory
Authors: Mahapatra Subhash 
Published: October 2020

AbstractRecently, a novel four-dimensional Gauss–Bonnet theory has been suggested as a limiting case of the originalD-dimensional theory with singular Gauss–Bonnet coupling constant$$\alpha \rightarrow \alpha /(D-4)$$α→α/(D-4). The theory is proposed at the level of field equations. Here we analyse this theory at the level of action. We find that the on-shell action and surface terms split into parts, one of which does not scale like$$(D-4)$$(D-4). The limiting$$D\rightarrow 4$$D→4procedure, therefore, gives unphysical divergences in the on-shell action and surface terms in four dimensions. We further highlight various issues related to the computation of counterterms in this theory.
Dually flat structures induced from monotone metrics on a two-level quantum state space
Authors: Fujiwara Akio 
Published: October 2020

AbstractThe notion of dually flatness is of central importance in information geometry. Nevertheless, little is known about dually flat structures on quantum statistical manifolds except that the Bogoliubov metric admits a global dually flat structure on a quantum state space $${{\mathcal {S}}}({{\mathbb {C}}}^d)$$

S
(

C

d

)

for any $$d\ge 2$$

d
≥
2

. In this paper, we show that every monotone metric on a two-level quantum state space $${{\mathcal {S}}}({{\mathbb {C}}}^2)$$

S
(

C

2

)

admits a local dually flat structure.
Subjectivité de la représentation du genre littéraire chez Jouri Tynianov et Mikhaïl Bakhtine: essai de définition et étude de textes
Authors: Garziano Svetlana 
Published: October 2020

Afin d’approfondir l’examen de la nature du genre littéraire et comme le présent volume porte en partie sur les questions du formalisme russe, cet article s’intéressera à l’expression de la subjectivité appliquée aux genres littéraires telle qu’elle est exposée dans quelques textes fondamentaux écrits par deux grands théoriciens du verbe russe : d’une part, il s’agit de Jouri Tynianov, l’un des principaux acteurs de l’OPOÏAZ, le fondateur du formalisme russe avec Victor Chklovski, Roman Jacobson et Boris Eïkhenbaum, et, d’autre part, c’est Mikhaïl Bakhtine qui a entamé son cheminement intellectuel au moment où « le formalisme était au faîte de sa gloire ».
Risk Factors and Timing of Acute Myocardial Infarction Associated With Pregnancy: Insights From the National Inpatient Sample
Authors: Balgobin Courtney A. , Zhang Xiaoyue , Lima Fabio V. , Avila Cecilia , Parikh Puja B. , Yang Jie , Stergiopoulos Kathleen 
Published: October 2020

Background
Pregnancy increases the risk of acute myocardial infarction (AMI). The purpose of this study was to examine timing and risk factors for AMI in pregnancy and poor outcome.

Methods and Results

National Inpatient Sample (2003–2015) was screened in pregnancy, labor and delivery, and postpartum. There were 11 297 849 records extracted with 913 instances of AMI (0.008%). One hundred eleven (12.2%) women experienced AMI during labor and delivery, 338 (37.0%) during pregnancy and most during the postpartum period (464; 50.8%). The prevalence of AMI in pregnancy has increased (
P
=0.0005). Most major adverse cardiovascular and cerebrovascular events occurred in the postpartum period (63.5%). Inpatient mortality was 4.5%. Predictors of AMI include known coronary artery disease (odds ratio [OR], 517.4; 95% CI, 420.8–636.2), heart failure (OR, 8.2; 95% CI, 1.9–35.2), prior valve replacement (OR, 6.4; 95% CI, 2.4–17.1), and atrial fibrillation (OR, 2.7; CI, 1.5–4.7;
P
<0.001). Risk factors of traditional atherosclerosis including hyperlipidemia, obesity, tobacco history, substance abuse, and thrombophilia were identified (
P
<0.001). Gestational hypertensive disorders (eclampsia OR, 6.0; 95% CI, 3.3–10.8; preeclampsia OR, 3.2; 95% CI, 2.5–4.2) were significant risk factors in predicting AMI. Risk factors associated with major adverse cardiovascular and cerebrovascular events included prior percutaneous coronary intervention (OR, 6.6; 95% CI, 1.4–31.2) and pre‐eclampsia (OR, 2.3; 95% CI, 1.3–3.9).

Conclusions
AMI is associated with modifiable, nonmodifiable, and obstetric risk factors. These risk factors can lead to devastating adverse outcomes and highlight the need for risk factor modification and public health resource initiatives toward the goal of decreasing AMI in the pregnant population.
Regional Right Ventricular Abnormalities Implicate Distinct Pathophysiological Conditions in Patients With Chronic Thromboembolic Pulmonary Hypertension
Authors: Moriyama Hidenori , Kawakami Takashi , Kataoka Masaharu , Hiraide Takahiro , Kimura Mai , Endo Jin , Kohno Takashi , Itabashi Yuji , Seo Yoshihiro , Fukuda Keiichi , Murata Mitsushige 
Published: October 2020

Background
Right ventricular (RV) dysfunction is a prognostic factor for cardiovascular disease. However, its mechanism and pathophysiology remain unknown. We investigated RV function using RV‐specific 3‐dimensional (3D)‐speckle‐tracking echocardiography (STE) in patients with chronic thromboembolic pulmonary hypertension. We also assessed regional wall motion abnormalities in the RV and chronological changes during balloon pulmonary angioplasty (BPA).

Methods and Results

Twenty‐nine patients with chronic thromboembolic pulmonary hypertension who underwent BPA were enrolled and underwent right heart catheterization and echocardiography before, immediately after, and 6 months after BPA. Echocardiographic assessment of RV function included both 2‐dimensional‐STE and RV‐specific 3D‐STE. Before BPA, global area change ratio measured by 3D‐STE was significantly associated with invasively measured mean pulmonary artery pressure and pulmonary vascular resistance (
r
=0.671 and
r
=0.700, respectively). Dividing the RV into the inlet, apex, and outlet, inlet area change ratio showed strong correlation with mean pulmonary artery pressure and pulmonary vascular resistance before BPA (
r
=0.573 and
r
=0.666, respectively). Only outlet area change ratio was significantly correlated with troponin T values at 6 months after BPA (
r
=0.470), and its improvement after BPA was delayed compared with the inlet and apex regions. Patients with poor outlet area change ratio were associated with a delay in RV reverse remodeling after treatment.

Conclusions
RV‐specific 3D‐STE analysis revealed that 3D RV parameters were novel useful indicators for assessing RV function and hemodynamics in pulmonary hypertension and that each regional RV portion presents a unique response to hemodynamic changes during treatment, implicating that evaluation of RV regional functions might lead to a new guide for treatment strategies.
Abstract 235: Hypertrophic Cardiomyopathy, a Disease of Altered Cardiac Energetics
Authors: Ranjbarvaziri Sara , Ellenberger Mathew , Kooiker Kristi , Fajardo Giovanni , Zhao Mingming , Schroer Alison , Woo Y Joseph Y , Ruppel Kathleen M , Spudich James A , Snyder Michael , Contrepois Kevin , Bernstein Daniel 
Published: October 2020

Hypertrophic cardiomyopathy (HCM) is a complex disease, the phenotypes of which are only partly explained by the biomechanical effects of individual genetic variants. At the cellular level, HCM sarcomeric mutations generally enhance maximal force production ultimately leading to higher energy demands. Despite significant advances in elucidating sarcomeric structure-function relationships, there is limited knowledge on the link between altered cardiac energetics and HCM phenotypes. In this work, we test the hypothesis that changes in cardiac energetics are a common pathway leading to the clinical pathophysiological phenotypes of HCM.
We performed a comprehensive multi-omic study of the molecular, ultrastructural, and functional features of HCM energetics using septal myectomy samples from 27 HCM patients and 13 normal controls (donor hearts). Combined mass spectrometry and RNA-Seq revealed dramatic alterations in multiple metabolic pathways,with major dysregulation in fatty acid metabolism leading to reduced acylcarnitines and accumulation of free fatty acids. Additionally, HCM hearts showed clear signs of global energetic decompensation manifested by a decrease in high energy phosphate metabolites (ATP, ADP, and PCr) and reduction in several mitochondrial genes involved in creatine kinase and ATP synthesis machinery. Quantitative electron microscopy showed a marked increase in severely damaged mitochondria with reduced cristae density, affecting 10-12% of total mitochondria, coinciding with reduced citrate synthase (CS) activity and mitochondrial respiration. These mitochondrial abnormalities were associated with elevated ROS and reduced antioxidant defenses along with insufficient mitophagic clearance.
Overall, our findings suggest that perturbed metabolic signaling and mitochondrial dysfunction are common pathogenic mechanisms in HCM. A central role for compromised energetics in HCM could also help explain the delayed age of onset of the clinical phenotype and present novel drug targets for attenuation of the clinical disease through reducing mitochondrial injury and improving function.
Abstract 264: Upstream and Downstream Regulators of Lysophosphatidic Acid Receptor 4 are Critical for Cardiac Differentiation and Repair
Authors: Cho Hyun-jai , Lee Jin-Woo , Lee Choon-Soo , Kim Hyo-Soo 
Published: October 2020

The therapeutic application of cell therapy to repair the damaged heart requires a comprehensive understanding of the process of cardiac differentiation of stem cells. We discovered a cardiac-specific marker, lysophosphatidic acid receptor 4 (LPAR4), which is G protein-coupled receptor (GPCR) and demonstrated its functional significance during cardiac differentiation. We screened GPCR expressing on mouse cardiac progenitor cells at differentiation day 3 compared to mouse undifferentiated pluripotent stem cells (PSCs). Among candidates, we identified LPAR4. We have found that in both mouse and human PSCs, LPAR4 has a transient expression pattern during cardiac differentiation. During in vitro differentiation of mouse and human PSCs toward cardiomyocytes, LPAR4 expression peaked for 3-5 days and then and declined immediately. Treatment with ODP (LPAR4 specific agonist) followed by p38MAPK blocker (SB203580) in the cardiac differentiation protocol significantly increased cardiac differentiation efficiency. Then we performed RNA sequencing to find transcription factors that regulate LPAR4. We screened 2-fold up-regulated transcription factors that related to cardiac differentiation during human iPSCs toward cardiomyocytes. The expression of LPAR4 is regulated by SOX17 expression, demonstrating that SOX17 is an upstream regulator of LPAR4. During cardiac differentiation, when knocking down SOX17 by siRNA, the expression of LPAR4 decreased as the expression of SOX17 mRNA decreased, resulting in no progression of cardiac differentiation. Besides, cardiac differentiation did not progress when SOX17 was overexpressed. SOX17 plays a role early in cardiac differentiation and that the expression should be reduced. However, it is assumed that sox17 lentivirus was gene-integrated and continued expression without decreasing expression. SOX17 overexpression needs further study. In conclusion, we demonstrated that LPAR4 is a novel cardiac progenitor cell marker and modulation of the upstream and downstream regulators shown functional significance during cardiac differentiation. Furthermore, our findings provide new insight into cell-free cardiac repair by the modulation of LPAR4 positive cells in the heart.
Funding Source: This study was supported by "Strategic Center of Cell and Bio Therapy for Heart, Diabetes & Cancer" (HI17C2085) through the Korea Health Industry Development Institute, funded by the Ministry of Health & Welfare, Republic of Korea.
Abstract 401: Head to Heart: Mental Health as a Precursor for Heart Disease in San Joaquin Muslim Population
Authors: Siddiqui Maha 
Published: October 2020

Introduction:
Islamophobia affects the mental health of the large San Joaquin (SJ) Muslim population leading to psychological distress and mental health concerns which can further lead to High Blood Pressure (HBP) and cardiovascular disease (CVD). SJ has a growing rate of Muslim immigrants who may be at risk for psychological distress and CVD.

Objectives:
Trainees conducted Kessler psychological distress tests, HBP and CVD screenings at mosques to reduce the risk of CVD and spread awareness about mental health, CVD and its implications in the Muslim population due to environmental racism in the most underserved county for health care, SJ.

Methods:
I trained medically ambitious low-income minority female high school students to conduct weekly Kessler psychological distress tests, blood pressure screenings and serve as a health technology coach. Each student monitored 2 hypertensive and psychological distressed patients of 40 hypertensive, psychological distressed, at risk for CVD and low-income Muslim residents. Kessler psychological distress tests and CVD screenings were conducted at all SJ mosques to spread awareness about mental health and heart health and track psychological distress and HBP in the Muslim community.

Findings:

-About 58% (304 of 527) of SJ Muslim population are at risk for CVD
-About 42% (221 of 527) of SJ Muslim population are Stage 1 hypertensive
-About 19% (98 of 527) of SJ Muslim population are Stage 2 hypertensive
-About 61% (319 of 527) of SJ Muslim population are hypertensive and psycologically distressed

Direct Outcomes:

-Youth learned the value of empathy, multiculturalism and service to disadvantaged communities through the program and volunteering
-Female empowerment and program students are determined to pursue medicine and address community concerns
-Improved patient provider trust
-Development of self advocacy for health in the Muslim communityIncreased awareness on CVD, HBP, and mental health among the Muslim communityIncreased participation of youth and females in an otherwise adult and male dominant environments (i.e. mosques)
-Awareness, education among Muslim community for better heart and mental health
-Better understanding in how to manage and seek referral for mental health concerns
Abstract 543: Clinical Development of Cardiac Reprogramming Gene Therapy
Authors: Zhou Huanyu , Lombardi Laura M , Reid Christopher A , Yang Jin , Srinath Chetan , Zeng Aliya , Leon Elena C , Qureshi Tawny N , Nettesheim Emily R , Xu Emma , Duclos Zoe , Liu Jun , Jones Samantha , Feathers Charles , Chung Tae Won , Jing Frank , Prince William , Lin JianMin , Hoey Timothy , Ivey Kathryn 
Published: October 2020

Heart failure affects an estimated 38 million people worldwide and is typically caused by cardiomyocyte (CM) loss or dysfunction. Although CMs have limited ability to regenerate, a large pool of non-myocytes, including cardiac fibroblasts (CFs), exist in the postnatal heart. In vivo reprogramming of non-myocytes into functional CMs is emerging as a potential new approach to treat heart failure and substantial proof-of-concept has been achieved in this new field. However, challenges remain in terms of clinical application. First, reported human reprogramming cocktails often consist of five to seven factors that require multiple AAV vectors for delivery. Thus, a less complex cocktail that is able to fit into one AAV vector is needed for this technology to impact human health. Second, the lack of specificity in AAV tropism further complicates the safety and regulatory landscape. A means to limit the expression of reprogramming factors to target cells is critical for maximizing long-term safety. Lastly, although promising studies in small animals have already been reported, safety and efficacy results in large animal MI models are critical to justify cardiac reprogramming in human clinical trials.
We have developed a novel human cardiac reprogramming cocktail that consists of only two transcription factors and one miRNA. This new cocktail has been engineered into a single AAV cassette to efficiently reprogram human CFs into cardiomyocytes. We also substantially improved transduction of hCFs through AAV capsid engineering and eliminated CMs expression through a microRNA de-targeting method. Moreover, our novel cardiac reprogramming gene therapy improved cardiac function in both rat and swine MI models upon delivery at various time-points after MI without inducing arrhythmias. Given these promising safety and efficacy results in larger animals, we endeavor to translate direct cardiac reprogramming for clinical application.
Abstract MP144: Identification of Epigenetic Regulators of Cardiac Hypertrophy by an Epigenome-wide Association Study in Mice
Authors: Rau Christoph D , Romay Milagros , Wong Eleanor , Tan Wilson , Lusis Aldons J , Foo Roger , Wang Yibin 
Published: October 2020

We previously reported a study of heart failure in a large cohort of inbred mouse strains, the Hybrid Mouse Diversity Panel (HMDP), treated with the beta-adrenergic agonist isoproterenol, which identified over 30 genome-wide significant loci for heart failure-related traits. Our approach combined systems-level tools with the benefits of a curated model organism population to identify genetic variations that drive heart failure.
We now expand this study into the epigenome. Recent research has demonstrated that DNA methylation affects the progression of cardiovascular phenotypes. This research suggests that DNA methylation may serve as an additional marker of genes involved in heart failure-associated phenotypes. Using Reduced Representational Bisulfite Sequencing, we profiled left ventricular tissue samples from 88 strains of the HMDP both before and after isoproterenol challenge (30 mg/kg/day for 21 days). We identified approximately 168,000 CpGs that vary across the panel and associated them with a set of phenotypes in both control and treated animals using the epigenome-wide association study (EWAS) algorithm MACAU. 179 significant associations were recovered at an FDR of 5%, including loci that associated pre-treatment CpG methylation with 19 different post-treatment phenotypes.

By combining these EWAS loci with information from the Wellcome Trust Mouse Genomes Resource and prior work done in the heart failure HMDP, we identify several high-confidence candidate genes, including
Coro1a
, a gene whose pre-treatment promoter methylation status predicts post-treatment wall thickening and
Eprs
, which predicts right ventricular weight post-treatment.
Mospd3
, a gene that was associated with right ventricular weight post-treatment in both EWAS and GWAS analyses was studied further using neonatal rat ventricular myocytes. This
in vitro
work demonstrates that
Mospd3
knockdown results in reduced cellular hypertrophy and changes to hypertrophy-related gene expression. Further analysis of the EWAS loci using
in vitro
and
in
vivo techniques will likely validate additional genes and elucidate how DNA methylation acts to regulate pathways underlying heart failure.
Ischemic Stroke Occurs Less Frequently in Patients With COVID-19
Authors: Bekelis Kimon , Missios Symeon , Ahmad Javaad , Labropoulos Nicos , Schirmer Clemens M. , Calnan Daniel R. , Skinner Jonathan , MacKenzie Todd A. 
Published: October 2020

Background and Purpose:
The impact of coronavirus disease 2019 (COVID-19) on the occurrence of ischemic stroke has been the subject of increased speculation but has not been confirmed in large observational studies. We investigated the association between COVID-19 and stroke.

Methods:
We performed a cross-sectional study involving patients discharged from a healthcare system in New York State, from January to April 2020. A mixed-effects logistic regression analysis and a propensity score–weighted analysis were used to control for confounders and investigate the association of COVID-19 with ischemic stroke. Similar techniques were used to detect the impact of concurrent COVID-19 infection on unfavorable outcomes for patients with stroke.

Results:
Among 24 808 discharges, 2513 (10.1%) were diagnosed with COVID-19, and 566 (0.2%) presented with acute ischemic stroke. Patients diagnosed with COVID-19 were at one-quarter the odds of stroke compared with other patients (odds ratio, 0.25 [95% CI, 0.16–0.40]). This association was consistent in all age groups. Our results were robust in sensitivity analyses, including propensity score–weighted regression models. In patients presenting with stroke, concurrent infection with severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) was associated with higher case-fatality (odds ratio, 10.50 [95% CI, 3.54–31.18]) and a trend towards increased occurrence of discharge to rehabilitation (odds ratio, 2.45 [95% CI, 0.81–1.25]).

Conclusions:
Using a comprehensive cross-section of patients from a large NY-based healthcare system, we did not identify a positive association between ischemic stroke and COVID-19. However, patients with stroke with COVID-19 had worse outcomes compared with those without, with over a 9-fold increase in mortality. Although no definitive conclusions can be reached from our observational study, our data do not support the concerns for an epidemic of stroke in young adults with COVID-19.
The Jewish Complex, Whose Complex Is It?
Authors: Cerminara Barbara 
Published: October 2020

Abstract
In 1934, attempting to extricate himself from the accusation of connivance with the Nazis, Jung conjectured about the existence of a Jewish complex. Recently, Jungian analyst Tirzah Firestone has argued that Jews suffer from a Jewish cultural complex which revolves around clusters of tribal traumatic experience. This discussion takes up from both Jung and Firestone addressing the question: The Jewish complex, whose complex is it? Stressing the relational element of Jung’s complex theory, developed into a theory of cultural complexes by Singer and Kimbles, the author of this paper, whose grandfather died in Auschwitz, places the Jewish complex among us Westerners, Jews and non-Jews. The Jewish complex is considered an affectively charged shared mental representation of a traumatic history, whose denouement is the Shoah, that affects us all. Cultural complexes such as the Jewish complex need to be understood relationally if there is to be any form of ‘resolution’.