bluuebunny/crossref_metadata_2025_split huggingface dataset:
Poster No. 133 Local TGF-beta sequestration by fibrillin-1 regulates vascular wall homeostasis in the thoracic aorta
Authors: de Backer Julie , de Leeuw Violette , Van Impe Mathias , Vanhomwegen Marine , Logghe Gerlinde , Oblinado Margie , Stampanoni Marco , Segers Patrick , Mosquera Laura Muino , Sakai Lynn , Sips Patrick 
Published: October 2022

Abstract

Introduction
Marfan syndrome (MFS) is caused by a defect in fibrillin-1, which binds TGF-beta via interaction with latent TGF-beta binding proteins (LTBPs). The role of TGF-beta in MFS is controversial.

Objectives
use dedicated mouse models for MFS, with defects interfering with TGF-beta binding and function, to gain insights into the role of TGF-beta signaling in aneurysm formation and dissection.

Material & methods
Mice lacking the binding site for LTBPs (Fbn1H1Δ/+ and Fbn1H1Δ/H1Δ), mice with a truncated fibrillin-1 (Fbn1GT-8/+), and mice with a combination (Fbn1GT-8/H1Δ) were subjected to cardiac ultrasound and ex vivo synchrotron X-ray imaging.

Results
Only Fbn1GT-8/H1Δ mice showed increased mortality (aortic rupture) starting at 4–5 months, whereas all other mice had a normal life span. Aortic root dilatation occurred both in Fbn1GT-8/+ and Fbn1GT-8/H1Δ mice at 6 months, but not in Fbn1H1D/+ or Fbn1H1Δ/H1Δ mice. Significant elastin fragmentation was observed in the thoracic aortic wall of Fbn1GT-8/+ mice, and to a larger extent in Fbn1GT-8/H1Δ mice. Surprisingly, localized elastin fragmentation was also found in the ascending aorta of Fbn1H1Δ/+ and Fbn1H1Δ/H1Δ mice, despite a lack of aortic aneurysm formation. Moreover, Fbn1H1Δ/H1Δ mice displayed more severe aortic wall damage.

Conclusion
Our data suggest that loss of LTBP binding to fibrillin-1 leads to the development of localized aortic microdissections in the absence of aortic aneurysm, and exacerbates the aortic wall morphology abnormalities in mice with truncated fibrillin-1. We therefore hypothesize that local TGF-beta sequestration is required to maintain aortic homeostasis.
Poster No. 134 Zebrafish as a tool to study cardiovascular effects caused by fibrillin impairment
Authors: de Backer Julie , de Rycke Karo , Caboor Lisa , Vermassen Petra , Sips Patrick 
Published: October 2022

Abstract

Introduction
Marfan syndrome (MFS) is the most common type of fibrillinopathy with a high predisposition to develop TAAD. A thorough understanding of the underlying mechanisms is still lacking, indicating a particular need for more flexible in vivo models to address this knowledge gap.

Objectives
We aimed to generate a relevant zebrafish model to gain insight into the molecular mechanisms relating fibrillin defects to the cardiovascular system.

Methods
The CRISPR/Cas9 system was used to systematically target the three different fibrillin genes (fbn1, fbn2a and fbn2b) in Tg(kdrl:GFP) reporter zebrafish. Time-lapse fluorescent microscopy was used to evaluate the cardiovascular phenotype.

Results
zebrafish lacking fbn1 and/or fbn2a do not show any cardiovascular phenotype during early-stage development. On the other hand, approximately 50% of homozygous fbn2b mutant (fbn2b-/-) zebrafish embryo's show a severe phenotype characterized by endocardial detachment, leading to vascular embolism and premature mortality at 7–9 dpf. Interestingly, the remaining fbn2b-/- zebrafish survive until adulthood, but during larval stages already develop a dilation of the bulbus arteriosus. The caudal vein of all fbn2b-/- embryos also develops abnormally as a cavernous structure lacking vessel integrity. This phenotype is resolved in embryos retaining normal blood flow and aggravated upon pharmacological inhibition of blood flow during development.

Conclusion
These data indicate that fbn2b-/- zebrafish model recapitulates cardiovascular complications, and can be considered as a relevant model to study the mechanisms underlying MFS pathogenesis. Our preliminary data suggest that there is an interplay between fibrillin deficiency and biomechanical signaling in the regulation of cardiovascular development.
Poster No. 139 Direct Oral Anticoagulant Use in the Treatment of Venous Thromboembolism Associated with Cancer
Authors: Carmo Francisca , Cabral Joana Martins , Magalhães Luísa 
Published: October 2022

Abstract
Venous thromboembolism (VTE) is a common cause of death and complications in patients with cancer. Choosing an anticoagulant is challenging because these patients are at high risk of recurrent VTE and bleeding. Major guidelines recommended the use of low-molecular-weight heparin (LMWH), but recent studies recommend consideration of direct anticoagulants (DOACs) in selected patients. However, their clinical use is limited by the increased risk of bleeding and interaction with other drugs.
Retrospective study, including patients followed since 2015 in VTE consultation, with cancer-associated VTE. Patients with an ECOG Performance Status Scale of 4 and with contraindications for anticoagulation were excluded. We reported the incidence of recurrent VTE and haemorrhage within the first year after anticoagulation. In this study, we compared the efficacy and safety of the use of DOACs versus LMWH in patients with cancer-associated VTE.
91 patients were included, 55% male, median age of 70 years and most frequent ECOG Performance Status Scale of 0 (44%). 65% of the patients were treated with DOACs. The most common cancers included: colorectal (26%), genitourinary (25%), haematological (10%) and upper gastrointestinal (9%). Were reported 6 recurrent VTE events (4 pulmonary embolisms, 2 deep vein thrombosis) and 6 minor bleeding events, without any major or fatal event. The occurrence of recurrent thromboembolic events or bleeding was not significantly different between patients treated with LMWH or DOACs.
In this real-world observational study, we confirm the efficacy and safety of the use of DOACs in the treatment of VTE associated with cancer in selected patients.
Poster No. 140 Major cardiovascular events in high cardiovascular risk patients submitted to non-cardiac surgery and its clinical determinants
Authors: Carvalho Mariana Ferreira , Gonçalves Carolina , Cabral Margarida , Fernandes Sara Lopes , Carvalho Rita Ribeiro , Guardado Jorge , Antunes Alexandre , Morais João 
Published: October 2022

Abstract

Introduction
Pre-operative cardiovascular assessment of patients with high ischaemic risk is fundamental to give the best perioperative management. Morbi-mortality is mainly due to patient-related risk and surgery-related risk. However, the risk scores are very heterogeneous and derived from non-cardiac populations, making them less accurate.

Purpose
The study aims to characterize a cohort of patients with high ischemic risk who underwent non-cardiac surgery and to identify predictors of perioperative major adverse cardiovascular events (MACE) defined by urgent revascularization, myocardial infarction (MI) and/or cardiac death, thromboembolism and acute limb ischemia.

Methods
A single-center retrospective observational analysis between January 2015 and August 2022 evaluated 356 patients. Eligibility criteria included: patients with high cardiovascular risk with previous diagnosis of cardiac disease, planned to be submitted to high-risk non-cardiac surgery, and perioperative follow-up at our center.

Results
A total of 356 patients with high cardiovascular risk undergoing NCS were eligible in the cohort. Perioperative MACE occurred in 4.5% of the patients. Predictors of MACE during perioperative period were older age (P &lt; 0.001), chronic pulmonary disease (P = 0.031), coronary artery disease (CAD) (P = 0.011) and valvular heart disease (P = 0.039). Diabetes and hypertension exhibited a neutral impact in these patients.

Conclusions
These results highlight the increased thrombotic risk inherent to major surgery in patients with high risk cardiovascular disease. Older age, previous diagnosis of chronic pulmonary disease, coronary artery disease, and valvular heart disease are predictors of MACE in patients submitted to non-cardiac surgery, providing incremental value for predicting these events. More studies are needed to further caracterize this population.x
Clinical Case 26—Is it possible to live with thrombosed left ventricular assist device (LVAD)?
Authors: Dračina Nina , Golubović Miodrag , Zdravković Ranko , Redžek Aleksandar , Todić Mirko , Preveden Andrej 
Published: October 2022

Abstract
LVAD HeartWare was implanted in a 63-year-old patient with end-stage dilated cardiomyopathy. The postoperative course was complicated by massive gastrointestinal (GI) bleeding that required surgical exploration of the GI tract.
For the next 1.5 years, the patient has significantly improved functional capacity with proper LVAD function. A month before the incident, an alarm indicating a pump malfunction was recorded. The patient presents with congestive symptoms and an altered sound of LVAD. Laboratory indicates seven times elevated LDH values, low HGB and INR 3.03. Thrombophilia tests were negative. Echo examination does not indicate pump thrombosis, but the pump parameters show increased energy consumption (&gt;6 W) and increased flow (&gt;7 L/min). A diagnosis of LVAD thrombosis was made.
Fibrinolytic therapy was contraindicated because of a history of GI bleeding, so a continuous infusion of heparin was started. Despite this, the patient's clinical condition deteriorates, and a decision was made to discontinue the LVAD, to prevent further hemolysis that led to acute kidney injury (AKI). The procedure was performed without endangering the patient.
Massive hemolysis, however, leads to the progressive development of AKI requiring CVVHDF. Global respiratory insufficiency develops and mechanical ventilation was started. After six days of intensive treatment, the patient recovered and was discharged home with a thrombosed pump.
For the next 2.5 years, the patient was in satisfactory condition during follow-ups, the pump was not explanted.
Even sophisticated medical devices carry with them risks for the patient's life despite adequate management.
Treatment of LVAD thrombosis depends on patient characteristics and pump-related factors.
NanoSPECT imaging reveals the uptake of 123I-labelled oxidized low-density lipoprotein in the brown adipose tissue of mice via CD36
Authors: Hosomi Kento , Kawashima Hidekazu , Nakano Atsushi , Kakino Akemi , Okamatsu-Ogura Yuko , Yamashita Yuki , Sasaoka Mai , Masuda Daisaku , Yamashita Shizuya , Chen Chu-Huang , Yuzuriha Shunsuke , Hosoda Hiroshi , Iida Hidehiro , Sawamura Tatsuya 
Published: October 2022

Abstract

Aims
The liver is the major organ shown to remove oxidized low-density lipoprotein (oxLDL) from the circulation. Given increased evidence that thermogenic adipose tissue has anti-effects, we used 123I-labelled oxLDL as a tracer to reveal oxLDL accumulation in the brown adipose tissue (BAT) of mice. We also explored the mechanisms of oxLDL accumulation in BAT.

Methods and results
We used high-resolution nanoSPECT/CT to investigate the tissue distribution of 123I-oxLDL and 123I-LDL (control) following intravenous injection into conscious mice. 123I-oxLDL distribution was discovered in BAT at an intensity equivalent to that in the liver, whereas 123I-LDL was detected mostly in the liver. Consistent with the function of BAT related to sympathetic nerve activity, administering anaesthesia in mice almost completely eliminated the accumulation of 123I-oxLDL in BAT, and this effect was reversed by administering β3-agonist. Furthermore, exposing mice to cold stress at 4°C enhanced 123I-oxLDL accumulation in BAT. Because in 123I-oxLDL, the protein of oxLDL was labelled, we performed additional experiments with DiI-oxLDL in which the lipid phase of oxLDL was fluorescently labelled and observed similar results, suggesting that the whole oxLDL particle was taken up by BAT. To identify the receptor responsible for oxLDL uptake in BAT, we analysed the expression of known oxLDL receptors (e.g. SR-A, CD36, and LOX-1) in cultured brown adipocyte cell line and primary brown adipocytes and found that CD36 was the major receptor expressed. Treatment of cells with CD36 siRNA or CD36 neutralizing antibody significantly inhibited DiI-oxLDL uptake. Finally, CD36 deletion in mice abolished the accumulation of 123I-oxLDL and DiI-oxLDL in BAT, indicating that CD36 is the major receptor for oxLDL in BAT.

Conclusion
We show novel evidence for the CD36-mediated accumulation of oxLDL in BAT, suggesting that BAT may exert its anti-atherogenic effects by removing atherogenic LDL from the circulation.
Parenthood and the gender division of labour across the income distribution: the relative importance of relative earnings
Authors: Dunatchik Allison 
Published: October 2022

AbstractThis study employs a gendered relative resource approach to examine whether the importance of relative resources varies by couples’ household income in shaping changes in the gender division of labour after first birth. Scholarship has long argued that the gender division of labour within different-sex couples is influenced by partners’ relative resources. However, couples face class-based constraints that may alter the relevance of relative resources in shaping changes in gender divisions of labour following the transition to parenthood. This study compares couples’ paid work and housework before and up to four years after first birth, using 28 waves of the British Household Panel Survey and the UK Household Longitudinal Study (N = 1,606 couples). I find that the effect of relative resources on changes in couple’s paid work and housework behaviour after first birth varies substantially by household income. Among higher-income couples, women’s paid work and housework time changes less among those with high relative earnings and more among those with low relative earnings, while men’s time allocation varies little after first birth. In contrast, among low-income couples, women’s paid work time and share decreases most after first among female breadwinners while their male partners’ paid work time increases substantially. These findings reflect the greater constraints that low-income parents face in reconciling work and family and highlight the need for greater attention to class interactions in the process of gender specialization in both research and work-family policy.
Restrictive cardiomyopathy: definition and diagnosis
Authors: Rapezzi Claudio , Aimo Alberto , Barison Andrea , Emdin Michele , Porcari Aldostefano , Linhart Ales , Keren Andre , Merlo Marco , Sinagra Gianfranco 
Published: October 2022

AbstractRestrictive cardiomyopathy (RCM) is a heterogeneous group of diseases characterized by restrictive left ventricular pathophysiology, i.e. a rapid rise in ventricular pressure with only small increases in filling volume due to increased myocardial stiffness. More precisely, the defining feature of RCM is the coexistence of persistent restrictive pathophysiology, diastolic dysfunction, non-dilated ventricles, and atrial dilatation, regardless of ventricular wall thickness and systolic function. Beyond this shared haemodynamic hallmark, the phenotypic spectrum of RCM is wide. The disorders manifesting as RCM may be classified according to four main disease mechanisms: (i) interstitial fibrosis and intrinsic myocardial dysfunction, (ii) infiltration of extracellular spaces, (iii) accumulation of storage material within cardiomyocytes, or (iv) endomyocardial fibrosis. Many disorders do not show restrictive pathophysiology throughout their natural history, but only at an initial stage (with an evolution towards a hypokinetic and dilated phenotype) or at a terminal stage (often progressing from a hypertrophic phenotype). Furthermore, elements of both hypertrophic and restrictive phenotypes may coexist in some patients, making the classification challenge. Restrictive pathophysiology can be demonstrated by cardiac catheterization or Doppler echocardiography. The specific conditions may usually be diagnosed based on clinical data, 12-lead electrocardiogram, echocardiography, nuclear medicine, or cardiovascular magnetic resonance, but further investigations may be needed, up to endomyocardial biopsy and genetic evaluation. The spectrum of therapies is also wide and heterogeneous, but disease-modifying treatments are available only for cardiac amyloidosis and, partially, for iron overload cardiomyopathy.
Modelling of fluid pressure migration in a pressure sensitive fault zone subject to cyclic injection and implications for injection-induced seismicity
Authors: Ji Yinlin , Zhang Wei , Hofmann Hannes , Chen Yuedu , Kluge Christian , Zang Arno , Zimmermann Günter 
Published: October 2022

SUMMARY
Fault zones often serve as the major fluid pathways in a variety of geo-energy systems, such as deep geothermal systems. However, injection-induced instability of faults can sometimes lead to large-magnitude earthquakes. Cyclic injection has thus been proposed as an alternative injection protocol to better manage and mitigate the associated seismic risks. The risks of injection-induced seismicity depend primarily on the extent and magnitude of the fluid pressure perturbation. When fluid is injected into a fault zone, the local fault permeability will be enhanced, which in turn promotes the migration of fluid along the fault. This nonlinear process is further complicated during cyclic injection via alternating the injection pressure. In this study, both numerical and analytical modelling are conducted to investigate cyclic fluid injection into a fault zone with pressure sensitive permeability, in which the local fault permeability changes as a function of the local effective stress. The match with laboratory-scale experimental and field-scale analytical results of cyclic fluid injection verifies the accuracy of the numerical model. The parametric study reveals that the injection pressure attenuation, quantified by the amplitude ratio and phase shift, is enhanced by a lower initial fault permeability, a smaller stress sensitivity coefficient and a shorter period of pressure cycle (i.e. a higher frequency). Besides, the amplitude of the pressure cycle has a negligible effect on the injection pressure attenuation. We also discuss the implications of our results for the less amenable far-field seismic hazard and post shut-in seismicity.
Celebrating 25 Years of Varicella Vaccination Coverage for Children and Adolescents in the United States: A Success Story
Authors: Elam-Evans Laurie D , Valier Madeleine R , Fredua Benjamin , Zell Elizabeth , Murthy Bhavini P , Sterrett Natalie , Harris LaTreace Q , Leung Jessica , Singleton James A , Marin Mona 
Published: October 2022

Abstract
Tracking vaccination coverage is a critical component of monitoring a vaccine program. Three different surveillance systems were used to examine trends in varicella vaccination coverage during the United States vaccination program: National Immunization Survey–Child, National Immunization Survey–Teen, and immunization information systems (IISs). The relationship of these trends to school requirements and disease decline was also examined. Among children aged 19–35 months, ≥1 dose of varicella vaccine increased from 16.0% in 1996 to 89.2% by the end of the 1-dose program in 2006, stabilizing around at least 90.0% thereafter. The uptake of the second dose was rapid after the 2007 recommendation. Two-dose coverage among children aged 7 years at 6 high-performing IIS sites increased from 2.6%–5.5% in 2006 to 86.0%–100.0% in 2020. Among adolescents aged 13–17 years, ≥2-dose coverage increased from 4.1% in 2006 to 91.9% in 2020. The proportion of adolescents with history of varicella disease declined from 69.9% in 2006 to 8.4% in 2020. In 2006, 92% of states and the District of Columbia (DC) had 1-dose daycare or school entry requirements; 88% of states and DC had 2-dose school entry requirements in the 2020–2021 school year. The successes in attaining and maintaining high vaccine coverage were paramount in the dramatic reduction of the varicella burden in the United States over the 25 years of the vaccination program, but opportunities remain to further increase coverage and decrease varicella morbidity and mortality.
A novel technique of STEM observation of TEM section using LVSEM and application of pathological diagnosis of renal biopsy
Authors: Nagumo Tasuku , Sakaue Mari , Wakatsuki Mone , Inoue Yuriko , Mukai Shumpei , Yamochi Toshiko , Takaki Takashi 
Published: October 2022

Abstract
The usefulness of the transmission electron microscope (TEM) for pathological diagnosis is apparent. However, high operating costs and other disadvantages have limited the ability to maintain and operate a TEM. In recent years, a general-purpose benchtop low-vacuum scanning electron microscope (LVSEM), which is inexpensive and easy to operate, has been developed and is expected to be applied in electron microscopic pathological diagnosis. To date, we have previously observed TEM ultrathin sections of Immunoglobulin A (IgA) nephropathy with a benchtop LVSEM using an ultra variable-pressure detector (UVD) and a newly developed holder for observing scanning transmission electron microscope (STEM) images (UVD-STEM holder) and compared the images with those obtained with typical TEM observations. We reported the results in the 53rd Annual Meeting of the Japanese Society for Clinical Molecular Morphology and the 64th Symposium of The Japanese Society of Microscopy and discussed the validity of the methods in the pathological diagnosis of IgA nephropathy and other renal diseases. As a result, we demonstrated the potential for pathological diagnosis using benchtop LVSEM. In this study, we similarly examined typical kidney diseases such as membranous nephropathy, lupus nephritis and amyloidosis. We could obtain sufficient data for the pathological diagnosis of IgA nephropathy, membranous nephropathy and lupus nephritis. However, it is difficult to detect amyloid fibres that are characteristic of amyloidosis. The development of this method is expected to expand the possibilities for pathological diagnosis using electron microscopy, including its application to other diseases.
Bayesian reconstruction of dark matter distribution from peculiar velocities: accounting for inhomogeneous Malmquist bias
Authors: Boruah Supranta S , Lavaux Guilhem , Hudson Michael J 
Published: October 2022

ABSTRACT
We present a Bayesian velocity field reconstruction algorithm that performs the reconstruction of the mass density field using only peculiar velocity data. Our method consistently accounts for the inhomogeneous Malmquist (IHM) bias using analytical integration along the line of sight. By testing our method on a simulation, we show that our method gives an unbiased reconstruction of the velocity field. We show that not accounting for the IHM bias can lead to significant biases in the Bayesian reconstructions. We applied our method to a peculiar velocity data set consisting of the SFI++ and 2MTF Tully–Fisher catalogues and the A2 supernovae compilation, thus obtaining a novel velocity reconstruction in the local Universe. Our velocity reconstructions have a cosmological power spectrum consistent with the theoretical expectation. Furthermore, we obtain a full description of the uncertainties on reconstruction through samples of the posterior distribution. We validate our velocity reconstruction of the local Universe by comparing it to an independent reconstruction using the 2M++ galaxy catalogue, obtaining good agreement between the two reconstructions. Using Bayesian model comparison, we find that our velocity model performs better than the adaptive kernel smoothed velocity with the same peculiar velocity data. However, our velocity model does not perform as well as the velocity reconstruction from the 2M++ galaxy catalogue, due to the sparse and noisy nature of the peculiar velocity tracer samples. The method presented here provides a way to include peculiar velocity data in initial condition reconstruction frameworks.