bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Carta sobre o Infinito de Espinosa Como Recepção da crítica de Crescas a Maimônides
Authors: Leone Alexandre 
Published: July 2021

Na Carta sobre o Infinito Espinosa cita a prova da existência de Deus feita por Hasdai Crescas (1340 - 1411), que fez a mais veemente crítica ao aristotelismo medieval judaico. Acrítica de Crescas começa pela refutação das 26 proposições que Maimônides usou para com elas provar a existência de um Deus radicalmente transcendente. As primeiras três negam a possibilidade do infinito atual. Crescas em sua crítica à terceira proposição argumenta em prol da existência da série infinita de causas e efeitos, entendendo a causa primeira como causa ontológica imante de a toda série e que é determinante para a existência dos infinitos efeitos. Para Crescas essa causa primeira simultânea aos seus infinitos efeitos é Deus. Eis a primeira formulação da imanência na filosofia judaica. Ler Espinosa a luz da crítica de Crescas a Maimônides faz emergir a relação de recepção que esse filósofo moderno mantém com a filosofia judaica medieval.
A Participação Judaica na Cartografia Medieval Maiorquina
Authors: Nogueira Magali Gomes 
Published: July 2021

O presente artigo tem como objetivo apresentar considerações a respeito das fontes utilizadas para a construção do Padrão Portulano, gênero cartográfico entendido como de vital importância para o desenvolvimento da ciência cartográfica, uma vez que essa construção resulta de um longo processo de compilação e comprovação de dados astronômicos e geográficos que foram sendo acumulados pelos estudiosos desde o inicio da escrita. Sendoconsiderado como um “Renascimento Cultural”, o momento de sua produção, os séculos XIII e XIV foi marcado por um intenso processo de Disputas entre as tradições que contribuíram para sua realização, os islâmicos, hebreus e cristãos. Disputas estas que se encontram em forma de livros e textos representados nas bibliotecas encontradas em Maiorca, entendida como local da última etapa desta produção, materializada no famoso “Atlas Catalão” e nasCartas Portulano maiorquinas.
Lasar Segall e Zygmunt Turkow: dos Groisse Gevins (a Sorte Grande)
Authors: Falbel Nachman 
Published: July 2021

Em 1945 o ator e dramaturgo judeu Zygmunt Turkow , que se encontrava há alguns anos no Brasil atuando junto ao circulo dramático da Biblioteca Israelita Brasileira Sholem Aleichemno Rio de Janeiro,obteve a colaboração do pintor Lasar Segall para a realização dos cenários e figurinos para a peça “Dos groisse gevins”(A sorte grande) do clássico escritor de línguaídiche Sholem Aleichem. O presente artigo visa dar a público a original correspondência composta de 12 cartas ,escritas em russo , até agora inédita, concernente ao bem sucedido evento artístico apresentado em 20 de novembro no Teatro Ginástico do Rio de Janeiro.
Línguas Maternas: sobre a Convivência do Judeu-Espanhol com o Hebraico em Israel
Authors: Held Michal 
Published: July 2021

Este artigo dispõe-se a explorar e interpretar narrativas pessoais de mulheres falantes do judeu-espanhol, criadas na atmosfera cultural e linguística na atualidade israelense. A pesquisa é baseada num enfoque que define a narrativa pessoal como multifacetada e portanto utiliza ferramentas multidisciplinares para examinar o material coletado numa perspectiva linguística, literária, folclórica, antropológica e sociológica. As narrativas, assim como a atividade do grupo que serve de estrutura conceitual devem ser considerados à luz da definição de Benedict Anderson para uma “comunidade imaginária”, como a reconstrução do imaginário do judeu-espanhol, tido como uma identidade imaginária baseada numa cultura que virtualmente não tem função hoje em dia. Do aspecto da etnicidade a principal questão é se e como as narrativas pessoais criadas por mulheres falantes do judeu-espanhol aqui e agora refletem a identidade coletiva e as concepções do grupo étnico sefardita.
O tráfico de mulheres e o submundo judaico no romance "Maasê Betabaat" [O relato do anel], de Ilan Sheinfeld
Authors: Steinberg Gabriel 
Published: July 2021

No romance Maassê Betabaat, Ilan Sheinfeld traça a trajetória de duas famílias que, ao longo de três gerações, estão unidas pelos destinos de um anel com poderes mágicos e que se deslocam desde a cidade de Danzig até Buenos Aires, cidade para a qual milhares de judeus se dirigiram no final do século XIX, atrás de novas oportunidades econômicas. Entre eles, chegaram também aqueles que, determinados a prosperar através da exploração da prostituição, para lá levaram centenas de mulheres que foram transformadas em escravas sexuais. Nesse romance, Esperanza Gants revela à sua filha um nebuloso e terrível segredo: o de que ela, sua mãe e sua avó tinham sido prostitutas judias.
Abstract 330: Liver-Specific Phospholipids Transfer Protein Activity Has Significant Contribution in Hepatocyte Apob-Containing Lipoprotein Production and in Plasma Lipoprotein Metabolism
Authors: Yazdanyar Amirfarbod , Jiang Xian-Cheng 
Published: July 2021

Atherosclerosis is the leading cause of death in western countries. Lipoprotein metabolism is closely related with the disease. ApoB-containing lipoproteins (BLp) are atherogenic particles, while, high density lipoproteins (HDL) are anti-atherogenic. Phospholipids Transfer Protein (PLTP) activity has important impact on BLp and HDL homeostasis. Animal studies, including general knock out (KO) and transgenic approaches, have shown pro-atherogenic properties for PLTP. However, the tissue specific function of PLTP remains mostly unknown. To address the impact of liver-specific expression of PLTP on lipoprotein metabolism, we have created two mouse models which either express PLTP specifically in the liver on a PLTP-null background or do not express PLTP in the liver (liver-specific PLTP KO) in a wild type background. In both models, our findings show that liver-specific PLTP is responsible for 25-30% of total plasma PLTP activity. Moreover, liver-specific PLTP expression model shows a remarkable increase in plasma levels of BLp, whereas liver-specific PLTP KO mice show significant reduction of BLp in plasma in compare to control group. These results further show the significant contribution of PLTP in BLp production.
We also found that HDL levels are slightly increased in the first model, while in liver-specific PLTP KO animals HDL levels are significantly decreased. In order to unravel the mechanism, we evaluated the apoB and triglyceride production rates after blocking the clearance of the particles. We found that liver-specific PLTP increases apoB (both apo48 and apoB100) and triglyceride (TG) secretion rates. Additionally, the study of the hepatocyte microsomal luminal content lipidation in the first model showed that in the presence of PLTP BLp lipidation, which reflects as higher level of TG in microsomal luminal content, is significantly higher than the control group. Our results indicate that liver-generated PLTP promotes atherogenic lipoprotein production and provides a rationale for liver-specific PLTP inhibition as a therapeutical approach for the treatment of atherosclerosis.
Abstract 397: Analysis of Cell Phenotype in Relation to TGFβ Treatment of Aortic Smooth Muscle Cells and Myofibroblasts Isolated from Aortas and Valves of Thoracic Aortic Aneurysm Patients with a Tricuspid or a Bicuspid Valve
Authors: Paloschi Valentina , Folkersen Lasse , Kurtovic Sanela , Wagsater Dick , Franco Cereceda Anders , Roy Joy , Eriksson Per 
Published: July 2021

Background

Thoracic aortic aneurysm (TAA) is a pathological widening of the aorta, due to degeneration of extracellular matrix (ECM) and loss of smooth muscle cells (SMCs). Bicuspid aortic valve (BAV) is a congenital disorder present in 1-2 % of the population which makes TAA associated with BAV a common complication. Previously we showed that aortas isolated from BAV and normal tricuspid aortic valve (TAV) patients are different both at gene and protein levels. Particularly, differences in the TGFβ pathway seem to be crucial players in aneurysm development, affecting matrix remodeling and wound healing. Since SMCs and myofibroblasts are the critical cells responsible for these activities, we evaluated different properties of the cells focusing on fibronectin (FN) and its spliced versions, a target gene of TGFβ. Interestingly, extra domain A of FN (EDA) was previously described for its roles in vascular morphogenesis, as well as in processes like migration and proliferation.

Methods and results

Biopsies from the thoracic aorta and Aortic valves were collected during Elective Aortic Valve Replacement Surgery. mRNA expression was analyzed in the ascending aorta by Affymetrix Exon arrays in patients with TAV (n=46) and BAV (n=77). Expression of EDA was found increased only in dilated aortas from TAV patients but not in BAV patients.
Primary SMCs were isolated with the explant outgrowth technique from aortas of BAV and TAV patients (n=15). Myofibroblasts were isolated by collagenase digestion from BAV and TAV valves (n=30). Cells were cultured and treated with TGFβ at a concentration of 20 ng/ml for 6h. TGFβ treatment influenced the splicing of FN and enhanced the formation of EDA-containing FN in SMCs from TAV patients but not in cells derived from BAV patients. We have not observed clear differences in SMC proliferation and migration. Myofibrolasts analysis is ongoing.

Conclusions

So far, our results suggest that despite a decreased EDA-fibronectin expression in BAV cells, the phenotype of SMCs isolated from BAV and TAV patients in culture does not differ. However, impaired TGFβ signaling that may result in the increased susceptibility of BAV patients to develop TAA could be due to effects on other cell types.
Abstract 63: CXCL8 Signaling Pathways and the Aortic Abdominal Aneurysm: The Oral CXCR2 Antagonist DF2156A Fully Abrogates Aneurysm Formation
Authors: Kokje Vivianne B , Dalman R L , Hamming J F , Lindeman J H 
Published: July 2021

An aneurysm of the abdominal aorta (AAA) is part of the atherososclerotic spectrum of diseases. The disease is characterized by a localized dilatation of the infrarenal artery and rupture of the weakened segment is now responsible for more than 15.000 annual deaths in the US alone. The pathology of AAA is complex and poorly understood. It is generally conceived that AAA is characterized by a localized general pro-inflammatory response and an accompanying protease imbalance that is held responsible for the progressive weakening of the aortic wall. The exact inflammatory pathways that drive aneurysm progression and that distinguish AAA from occlusive atherosclerotic disease have not yet been identified. We previously reported a 21-fold increase in CXCL8 mRNA expression and an approx. 300-fold increase in CXCL8 protein levels in human AAA, as compared to human occlusive atherosclerotic disease (p<0.001); suggesting that activation of the CXCL8/CXCR1-2 axis is a distinctive feature of AAA.
We now performed a histological and protein analysis of human AAA and human occlusive atherosoclerotic disease, showing abundant presence of the CXCL8 receptors CXCR1 and 2 as well as increased ERK phosphorylation in AAA. Evaluation on cellular level identified abundant neutrophils (fully absent in atherosoclerosis) as well as increased neovascularization as clear distinctive features of AAA, a finding that is consistent with increased CXCL8 signaling. To test a putative role of CXCL8/CXCR1-2 system in AAA we next tested whether the oral CXCR2 antagonist DF2156A prevents aneurysm formation in the elastase model, a well established model of the disease. This study showed that a once daily dose of 15mg/kg DF2156A fully abrogates aneurysm formation in the elastase model (71.86% aortic diameter growth in 14 days (SEM 4.88) in untreated animals vs. 17.66% growth (SEM 1.71) in animals treated with DF2156A) (p<0.001).
In conclusion, these studies identify activation of the CXCL8/CXCR1-2 pathway as a distinctive feature of AAA and characterize this pathway as a potential target for the stabilization of AAA.
Abstract 128: Serum Anti-MAA Antibody Titers are Associated with Acute Myocardial Infarction and MMP-9
Authors: Ahmed Faisal , Duryee Michael J , Shurmur Scott W , Johnston Michael D , Hunter Carlos D , Thiele Geoffrey M , Anderson Daniel 
Published: July 2021

Introduction
Atherosclerotic plaque rupture is the leading cause of acute myocardial infarction (AMI). Malondialdehyde acetaldehyde (MAA) modified proteins have recently been implicated in this process by their ability to initiate inflammatory responses. Matrix metalloproteinase 9 (MMP-9) is increased following AMI and has been associated with the disease due to its ability to degrade the fibrotic cap that forms on some plaques.

Objective
The purpose of this study was to evaluate the relationship between MMP-9 and anti-MAA antibody isotypes in patients experiencing acute myocardial infarction (AMI).

Methods
Serum samples from AMI patients (n=10) were collected and tested for the presence of anti-MAA antibody isotypes, peak CK, peak troponin, and MMP-9 levels. Samples were collected at the time of AMI, 24 and 48 hours post event. Data was correlated to determine relationships with antibody isotypes directed against MAA protein antigens.

Results
MMP-9 increased significantly from the initial presentation at 24 hours post-AMI (p=0.006) and 48 hours post-AMI (p= 0.044). Anti-MAA IgM decreased significantly (p= 0.021) between initial and 24 hours post AMI. A similar significant decrease was observed for anti-MAA IgG (p= 0.006). Anti-MAA IgA levels did not change significantly post-AMI. Significant correlations were demonstrated between peak CK and anti-MAA IgG 24 hours post AMI (r= -0.819, p= 0.013), between peak troponin and anti-MAA IgG 24 hours post AMI (r= -0.860, p= 0.006) and between MMP-9 levels 24 hours post AMI and anti-MAA IgM levels 24 hours post MI ( r= 0.0712, p=0.021).

Conclusions
The negative correlation of anti-MAA IgG to cardiac enzymes is suggestive that myocardial infarction and tissue necrosis results in the release of the MAA antigen from infarcted myocardium and clearance of anti-MAA antibodies. Additionally, anti-MAA IgM and MMP-9 are positively correlated with each other 24 hours post-AMI, suggesting that anti-MAA IgM titers may correlate to the severity of the AMI and thus CAD.

Implications
Anti-MAA antibodies might serve as important biomarkers of impending atherosclerotic plaque rupture and subsequent AMI and warrants further investigation in a larger cohort of patients.
Abstract 13: Macrophage Erk5 Activation Induced by Apoptotic Cells and Statins Promotes Efferocytosis and Inhibits Atherosclerosis Formation
Authors: Heo Kyungsun , Cushman Hannah , Woo Chang-Hoon , Akaike Masashi , Wang Xin , Morrell Craig N , Fujiwara Keigi , Abe Jun-ichi 
Published: July 2021

Backgrounds
Defective efferocytosis (phagocytic clearance of dying cells) is critically linked to progression of advanced atherosclerotic lesions. Although it has been well known that efferocytosis is processed by molecules including eat-me and find-me signals, it is unclear how efferocytosis becomes defective in advanced lesion.

Methods and Results

Here, we found that bone marrow-derived macrophages (BMDM) from macrophage-specific ERK5 knockout (ERK5

fl/fl

LysM
Cre
+/-
; ERK5-MKO) mice reduced mRNA and proteins levels of efferocytosis-related signaling molecules such as Mer-tK, C1qa, C1qb, C1qc, Gas6, Mfg-e8, Thbs1, and Anxa1 compared with BMDM from non-transgenic control (NLC) mice. Interestingly, addition of apoptotic cells and pitavastatin activate ERK5 kinase activity and increase opsonins, eat-me and find-me signals, and phagocytic capacity toward apoptotic cells in normal macrophage, but macrophages from ERK5-MKO failed to respond in this manner. ERK5-MKO crossed to LDLR
-/-
mice and fed a high cholesterol diet for 16-week accelerated atherosclerosis formation with an increased level of apoptotic cell accumulation and necrotic core formation, which was accompanied by a significant reduction in collagen content and fibrous cap thickness. We also found lower levels of expression for Mfg-e8 and Thbs1 in the advanced necrotic core of ERK5-MKO mice compared to NLC mice.

Conclusion
Our study shows that apoptotic cells and statins-activated ERK5 plays a key role in coordinating the process of efferocytosis. Our results provide a mechanistic understanding of the clinically well-described cardiac risk of acute atherothrombotic events in advanced lesions.
1
Abstract 144: A20 Inhibits Pathologic Interferon-? Signaling in Smooth Muscle Cells to Prevent Atherosclerotic Vascular Disease
Authors: Moll Herwig P , Lee Andy , Ferran Christiane 
Published: July 2021

The pleiotropic cytokine Interferon-γ (IFNγ), best known for its anti-viral and immunomodulatory activities, also demonstrates pro-atherogenic effects. Implication of IFNγ in the pathogenesis of atherosclerosis results in part from the upregulation of a number of pro-inflammatory interferon stimulated genes (ISGs) in vascular smooth muscle cells (SMC). Hence, strategies to reduce IFNγ signaling are of particular interest to reduce or prevent pathologic vascular remodeling associated with atherosclerotic disease, for instance transplant arteriosclerosis.
We discovered that the anti-inflammatory and vasculoprotective protein A20 inhibits IFNγ signaling and thus the expression of ISG in vitro in human coronary artery SMC, and in vivo in vascular allografts. The aim of this study was to unveil the mechanism(s) of A20 mediated inhibition of IFNγ signaling.
Adenovirus-mediated overexpression of A20 in SMC significantly decreased mRNA and protein levels of signal transducer and activator of transcription 1 (STAT1), the key mediator of IFNγ signaling, as a result of lower transcription. Moreover, overexpression of A20 in SMC also efficiently inhibited activating Y701 phosphorylation of STAT1, through a mechanism possibly implicating A20 binding to STAT1, as confirmed by co-immunoprecipitation. As expected, overexpression of A20 also inhibited NF-κB activation in SMC, which is required for full-blown IFNγ responses. Indeed, we confirmed that inhibition of NF-κB by overexpression of its inhibitor, IκBα also quenched upregulation of ISGs in SMC, albeit without down-regulating STAT1.
Overall, our results identify A20 as a potent inhibitor of IFNγ signaling in SMC through several non-mutually exclusive mechanisms. This novel function of A20 in SMC further qualifies its atheroprotective properties and supports the pursuit of A20-based therapies for the cure of atherosclerotic vascular disease.
Abstract 157: Association of Cholesterol Profile to the Number of Vessels Involved with Coronary Artery Disease
Authors: Misra Neeladri , Kim Woo Sung , Scavina Michael , Ross Jill 
Published: July 2021

Introduction
The cholesterol profile is an important modifiable risk factor for CAD and our understanding of atherosclerosis has helped develop drugs that have significantly impacted treatment outcomes of CAD by lowering cholesterol levels. A study to find a correlation between the cholesterol profile and the number of vessels involved with CAD was our objective.

Hypothesis
Patients with significant CAD (defined as >50% stenosis on coronary angiography) in 2 or more vessels had worse cholesterol profiles compared to single vessel. A subset of the study looked to see if the use of statins affected the severity of CAD.

Methods
A retrospective review of 498 patients from our hospitals cardiac registry was done. The cholesterol profile of these patients done either during the admission for cardiac catherization or the most recent one was used to correlate. The catheterization reports were reviewed to find the number of vessels involved with >50% stenosis and a CAD severity score was calculated using the gensini scoring system. We also reviewed the patients medication reconciliation forms to see if they had been on statins.

Results
We could not correlate between the number of vessels affected with significant CAD and the cholesterol profile. Using One way ANOVA analysis neither the Tc/HDL ratio ( p value 0.692) or LDL (p value=0.458) or the HDL levels( p value=0.588) had any association to the number of coronary vessels affected with CAD. In our study subset, the use of statins did not lower the gensini scores significantly as compared to patients who were not on statins (p value 0.95).

Conclusions
The cholesterol profile bears no correlation with the number of vessels affected by CAD. Based on our findings, taking statins did not significantly influence the severity of CAD.
Abstract 18: The Effect of Lipid Modification on Peripheral Arterial Disease after Endovascular Intervention Trial (ELIMIT)
Authors: Brunner Gerd , Yang Eric Y , Kumar Anirudh , Wensheng Sun , Salim Salim S , Negi Smita , Murray Tyler , Lin Peter H , Hoogeveen Ron C , Chen Changyi , Kougias Panagiotis , Taylor Addison , Lumsden Alan B , Nambi Vijay , Ballantyne Christie M , Morrisett Joel D 
Published: July 2021

BACKGROUND
The Effect of Lipid Modification on Peripheral Arterial Disease after Endovascular Intervention Trial (ELIMIT), a prospective double-blind randomized study, was designed to determine over 24-months, the effects of triple drug lipid modification therapy versus mono therapy on the progression of atherosclerotic lesions in the distal superficial femoral artery (SFA), as assessed by 3.0T magnetic resonance imaging (MRI).

METHODS
A total of 95 patients were randomized to either mono therapy with simvastatin (40mg) or triple therapy with simvastatin (40mg), extended-release niacin (1.5g), and ezetimibe (10mg). MR imaging was performed at baseline, 6-, 12-, and 24-months. SFA wall, lumen, and total vessel volumes were quantified using inter-visit co-registered proton-density-weighted turbo spin echo MRI sequences. MRI derived SFA parameters and lipids were analyzed with multi-level models and non-parametric tests, respectively.

RESULTS
Baseline characteristics did not differ between mono and triple therapy groups, except for ethnicity (Table). There was no difference in adverse cardiovascular events between groups (p=0.99). SFA wall, lumen, and vessel volumes increased non-significantly for both groups between baseline and 24-months. Non-high-density lipoprotein cholesterol showed a larger reduction in triple therapy compared with mono therapy at 12-months (p=0.01).

CONCLUSION
Despite improved atherogenic lipid profiles, there was no significant difference between mono therapy with simvastatin and triple therapy with simvastatin, extended-release niacin, and ezetimibe for the 24-month changes in total SFA wall, lumen, and vessel volumes.