Como fazer carreira em publicidade com Massumi, Shaviro e Whitehead: cinema e acontecimento comunicacional / How to get ahead in advertising with Massumi, Shaviro and Whitehead: cinema and communicational event / Cómo triunfar en publicidad con Massumi, Shaviro y Whitehead: cine y evento comunicacional

Cinema é comunicação? Ou apenas em certas circunstâncias? E, nessas circunstâncias, estaríamos diante de que natureza de evento? Um "acontecimento comunicacional"? A partir do detalhamento do conceito de "corpo cinemático" de Shaviro, da "intensidade das imagens" de Massumi e da fenomenologia de Whitehead faremos um Estudo de Caso: o evento proporcionado pela exibição do filme How to Get Ahead in Advertising [Como Fazer Carreira em Publicidade] (1989) para uma classe de graduação do curso de Publicidade e Propaganda. Efeitos ideológicos por meios não ideológicos (afetos, intensidades e sentimentos) seriam os resultantes dos acontecimentos comunicacionais?

Could cinema provide communication? Or only in certain circumstances? And under these circumstances, what kind of event would we be facing? A "communicational event"? From the details of Shaviro's concept of "cinematic body", Massumi's "image intensity" and Whitehead's phenomenology, we will make a case study: the event provided by the exhibition of the film How to Get Ahead in Advertising (1989) to a graduate class of the Advertising and Propaganda course. Are ideological effects through non-ideological means (affections, intensities, and feelings) the ones resulting from communicational events?

¿El cine es comunicación? ¿O solo en determinadas circunstancias? Y en estas circunstancias, ¿a qué tipo de evento nos enfrentaríamos? ¿Un "evento comunicacional"? A partir de los detalles del concepto de "cuerpo cinematográfico" de Shaviro, la "intensidad de la imagen" de Massumi y la fenomenología de Whitehead, haremos un estudio de caso: el evento que brinda la exhibición de la película How to Get Ahead in Advertising [Cómo Triunfar en Publicidad] (1989) a un graduado clase del curso de Publicidad y Propaganda. ¿Los efectos ideológicos a través de medios no ideológicos (afecciones, intensidades y sentimientos) son el resultado de eventos comunicacionales?

Decoding the radiomic and proteomic phenotype of epicardial adipose tissue associated with adverse left atrial remodelling and post-operative atrial fibrillation in aortic stenosis.

AIMS: Epicardial adipose tissue (EAT) volume and attenuation on computed tomography (CT) have been associated with atrial fibrillation. Beyond these conventional CT measures, radiomics allows extraction of high-dimensional data and deep quantitative adipose tissue phenotyping, which may capture its underlying biology. We aimed to explore the EAT proteomic and CT-radiomic signatures associated with impaired left atrial (LA) remodelling and post-operative atrial fibrillation (POAF). METHODS AND RESULTS: We prospectively included 132 patients with severe aortic stenosis with no prior atrial fibrillation referred for aortic valve replacement. Pre-operative non-contrast CT images were obtained for extraction of EAT volume and other radiomic features describing EAT texture. The LA function was assessed by 2D-speckle-tracking echocardiography peak atrial longitudinal strain and peak atrial contraction strain. The EAT biopsies were performed during surgery for proteomic analysis by sequential windowed acquisition of all theoretical fragment ion mass spectra (SWATH-MS). The POAF incidence was monitored from surgery until discharge. Impaired LA function and incident POAF were associated with EAT up-regulation of inflammatory and thrombotic proteins, and down-regulation of cardioprotective proteins with anti-inflammatory and anti-lipotoxic properties. The EAT volume was independently associated with LA enlargement, impaired function, and POAF risk. On CT images, EAT texture of patients with POAF was heterogeneous and exhibited higher maximum grey-level values than sinus rhythm patients, which correlated with up-regulation of inflammatory and down-regulation of lipid droplet-formation EAT proteins. The CT radiomics of EAT provided an area under the curve of 0.80 (95% confidence interval: 0.68-0.92) for discrimination between patients with POAF and sinus rhythm. CONCLUSION: Pre-operative CT-radiomic profile of EAT detected adverse EAT proteomics and identified patients at risk of developing POAF.

Reduced blood pressure in sickle cell disease is associated with decreased angiotensin converting enzyme (ACE) activity and is not modulated by ACE inhibition.

BACKGROUND: Sickle cell disease (SCD) incurs vaso-occlusive episodes and organ damage, including nephropathy. Despite displaying characteristics of vascular dysfunction, SCD patients tend to present relatively lower systemic blood pressure (BP), via an unknown mechanism. We investigated associations between BP and renin-angiotensin-system (RAS) components in SCD and determined whether an inhibitor of angiotensin converting enzyme (ACE; often used to slow SCD glomerulopathy) further modulates BP and RAS components in a murine model of SCD. METHODS: BP was compared in human subjects and mice with/without SCD. Plasma angiotensin II, ACE and renin were measured by immunoassay. BP was reevaluated after treating mice with enalapril (25 mg/kg, 5x/week) for 5 weeks; plasma and organs were stored for angiotensin II and ACE activity measurement, and quantitative real-time PCR. RESULTS: Diastolic BP and systolic BP were significantly lower in patients and mice with SCD, respectively, compared to controls. Reduced BP was associated with increased plasma renin and markers of kidney damage (mice) in SCD, as well as significantly decreased plasma ACE concentrations and ACE enzyme activity. As expected, enalapril administration lowered BP, plasma angiotensin II and organ ACE activity in control mice. In contrast, enalapril did not further reduce BP or organ ACE activity in SCD mice; however, plasma angiotensin II and renin levels were found to be significantly higher in enalapril-treated SCD mice than those of treated control mice. CONCLUSION: Relative hypotension was confirmed in a murine model of SCD, in association with decreased ACE concentrations in both human and murine disease. Given that ACE inhibition has an accepted role in decreasing BP, further studies should investigate mechanisms by which ACE depletion, via both Ang II-dependent and alternative pathways, could contribute to reduce BP in SCD and understand how ACE inhibition confers Ang II-independent benefits on kidney function in SCD.

Heme induces significant neutrophil adhesion in vitro via an NFκB and reactive oxygen species-dependent pathway.

Intravascular hemolysis, a major manifestation of sickle cell disease (SCD) and other diseases, incurs the release of hemoglobin and heme from red blood cells, in turn triggering inflammatory processes. This study investigated the in vitro effects of heme, a major inflammatory DAMP, on the adhesive properties of isolated human neutrophils. Heme (20 and 50 µM) significantly increased the adhesion of neutrophils to fibronectin and to recombinant ICAM-1, under static conditions, even more efficiently than the potent pro-inflammatory cytokine, tumor necrosis factor-α (TNF); a microfluidic assay confirmed that heme stimulated neutrophil adhesion under conditions of shear stress. Heme-induced neutrophil adhesion was associated with the increased activities, but not expressions, of the Mac-1 and LFA-1 integrin subunits, CD11b and CD11a, on the cell surface. Notably, heme (50 µM) significantly induced NFκB translocation in neutrophils, and inhibition of NFκB activity with the BAY11-7082 molecule abolished heme-induced cell adhesion to fibronectin and significantly decreased CD11a activity. Flow cytometric analysis demonstrated major reactive oxygen species (ROS) generation in neutrophils following heme stimulation that could be inhibited by the antioxidant, α-tocopherol, and by BAY11-7082. Furthermore, co-incubation with α-tocopherol abrogated both heme-stimulated neutrophil adhesion and CD11a/CD11b activation. Thus, our data indicate that heme, at clinically relevant concentrations, is a potent activator of neutrophil adhesion, increasing the ligand affinity of the ß2 integrins via a mechanism that may be partially mediated by an NFkB-dependent pathway and the generation of ROS. Given the fundamental role that the adhesion of neutrophils to the vascular wall plays in SCD vaso-occlusion and other vascular inflammatory processes, our findings provide further evidence that cell-free heme is a major therapeutic target in the hemolytic diseases.

Prevalence, multimodality imaging characterization, and mid-term prognosis of quadricuspid aortic valves: an analysis of eight cases, based on 160 004 exams performed during 12 years in a tertiary care hospital.

AIMS: Quadricuspid aortic valve (QAV) is a rare abnormality, which may cause aortic regurgitation (AR) requiring surgical intervention in some patients. The characteristics associated with aortic valve functional degeneration in patients with QAV are still unknown. The aim of this study is to describe QAV prevalence, characterize the disease by multimodality imaging, evaluate predictors of severe AR, and assess mid-term prognosis. METHODS AND RESULTS: Retrospective search in imaging exams database of one tertiary centre, for patients diagnosed with QAV between January 2007 and September 2019. QAV was characterized by cardiac computed tomography, transthoracic/transoesophageal echocardiography, and cardiac magnetic resonance. A total of 160 004 exams were reviewed and eight patients with QAV were identified (50% men, mean age 53.5 ± 10.7 years). The prevalence of QAV was 0.005%. During a median follow-up of 52 months (interquartile range 16-88), there were no deaths. Seven patients (88%) had pure AR (three severe, one moderate, and three mild) and one patient (12%) had moderate AR and moderate aortic stenosis. Three patients (38%) with severe AR underwent valve surgery (two replacements and one repair). Analysis of predictors of severe AR was not statistically significant. CONCLUSION: QAV is a rare congenital cardiac defect, with a prevalence of 0.005% in our study. Its predominant functional abnormality was regurgitation and about one-third of the patients required aortic valve surgery. Multimodality imaging may play a pivotal role in assessing patients with QAV with significant valve dysfunction or associated congenital heart disease and improve their treatment strategy.

Influence of EPICardial adipose tissue in HEART diseases (EPICHEART) study: Protocol for a translational study in coronary atherosclerosis.

INTRODUCTION: Accumulation of epicardial adipose tissue (EAT) is associated with coronary artery disease (CAD) and increased risk of coronary events in asymptomatic subjects and low-risk patients, suggesting that EAT promotes atherosclerosis in its early stage. Recent studies have shown that the presence of CAD affects the properties of adjacent EAT, leading to dynamic changes in the molecular players involved in the interplay between EAT and the coronary arteries over the history of the disease. The role of EAT in late-stage CAD has not been investigated. OBJECTIVES: In a comparative analysis with mediastinal and subcutaneous adipose tissue, we aim to investigate whether the volume of EAT assessed by computed tomography and its proteome assessed by SWATH-MS mass spectrometry are associated with late stages of CAD in an elderly cohort of severe aortic stenosis patients. METHODS: The EPICHEART study (NCT03280433) is a prospective study enrolling patients with severe degenerative aortic stenosis referred for elective aortic valve replacement, whose protocol includes preoperative clinical, nutritional, echocardiographic, cardiac computed tomography and invasive coronary angiographic assessments. During cardiac surgery, samples of EAT and mediastinal and subcutaneous thoracic adipose tissue are collected for proteomics analysis by SWATH-MS. In addition, pericardial fluid and peripheral and coronary sinus blood samples are collected to identify circulating and local adipose tissue-derived biomarkers of CAD. CONCLUSION: We designed a translational study to explore the association of EAT quantity and quality with advanced CAD. We expect to identify new biochemical factors and biomarkers in the crosstalk between EAT and the coronary arteries that are involved in the pathogenesis of late coronary atherosclerosis, especially coronary calcification, which might be translated into new therapeutic targets and imaging tools by biomedical engineering.

Epicardial adipose tissue volume and annexin A2/fetuin-A signalling are linked to coronary calcification in advanced coronary artery disease: Computed tomography and proteomic biomarkers from the EPICHEART study.

BACKGROUND & AIMS: The role of epicardial adipose tissue (EAT) in the pathophysiology of late stage-coronary artery disease (CAD) has not been investigated. We explored the association of EAT volume and its proteome with advanced coronary atherosclerosis. METHODS: The EPICHEART Study prospectively enrolled 574 severe aortic stenosis patients referred to cardiac surgery. Before surgery, EAT volume was quantified by computed tomography (CT). During surgery, epicardial, mediastinal (MAT) and subcutaneous (SAT) adipose tissue samples were collected to explore fat phenotype by analyzing the proteomic profile using SWATH-mass spectrometry; pericardial fluid and peripheral venous blood were also collected. CAD presence was defined as coronary artery stenosis ≥50% in invasive angiography and by CT-derived Agatston coronary calcium score (CCS). RESULTS: EAT volume adjusted for body fat was associated with higher CCS, but not with the presence of coronary stenosis. In comparison with mediastinal and subcutaneous fat depots, EAT exhibited a pro-calcifying proteomic profile in patients with CAD characterized by upregulation of annexin-A2 and downregulation of fetuin-A; annexin-A2 protein levels in EAT samples were also positively correlated with CCS. We confirmed that the annexin-A2 gene was overexpressed in EAT samples of CAD patients and positively correlated with CCS. Fetuin-A gene was not detected in EAT samples, but systemic fetuin-A was higher in CAD than in non-CAD patients, suggesting that fetuin-A was locally downregulated. CONCLUSIONS: In an elderly cohort of stable patients, CCS was associated with EAT volume and annexin-A2/fetuin-A signaling, suggesting that EAT might orchestrate pro-calcifying conditions in the late phases of CAD.

Valve-in-Valve Transcatheter Aortic Valve Implantation Using Fluoroscopic Guidance for Late Failure of the Bioprosthetic Bentall Conduit BioValsalva™ Vascutek.

We describe one of the first-in-human cases of valve-in-valve transcatheter aortic valve implantation (TAVI) using fluoroscopic-only guidance for the treatment of late failure of a bio-prosthetic Bentall conduit, the BioValsalva™ Vascutek (Vascutek Terumo, Renfrewshire, Scotland), using a self-expandable heart valve prosthesis (CoreValve™ Evolut™ R, Medtronic, Dublin Ireland).

Attenuation of TNF-induced neutrophil adhesion by simvastatin is associated with the inhibition of Rho-GTPase activity, p50 activity and morphological changes.

Neutrophil adhesion to the vasculature in response to potent inflammatory stimuli, such as TNF-α (TNF), can contribute to atheroprogression amongst other pathophysiological mechanisms. Previous studies have shown that simvastatin, a statin with known pleiotropic anti-inflammatory properties, can partially abrogate the effects of TNF-induced neutrophil adhesion, in association with the modulation of ß2-integrin expression. We aimed to further characterize the effects of this statin on neutrophil and leukocyte adhesive mechanisms in vitro and in vivo. A microfluidic assay confirmed the ability of simvastatin to inhibit TNF-induced human neutrophil adhesion to fibronectin ligand under conditions of shear stress, while intravital imaging microscopy demonstrated an abrogation of leukocyte recruitment by simvastatin in the microvasculature of mice that had received a TNF stimulus. This inhibition of neutrophil adhesion was accompanied by the inhibition of TNF-induced RhoA activity in human neutrophils, and alterations in cell morphology and ß2-integrin activity. Additionally, TNF augmented the activity of the p50 NFκB subunit in human neutrophils and TNF-induced neutrophil adhesion and ß2-integrin activity could be abolished using pharmacological inhibitors of NFκB translocation, BAY11-7082 and SC514. Accordingly, the TNF-induced elevation of neutrophil p50 activity was abolished by simvastatin. In conclusion, our data provide further evidence of the ability of simvastatin to inhibit neutrophil adhesive interactions in response to inflammatory stimuli, both in vivo and in vitro. Simvastatin appears to inhibit neutrophil adhesion by interfering in TNF-induced cytoskeletal rearrangements, in association with the inhibition of Rho A activity, NFκB translocation and, consequently, ß2-integrin activity.

Comparison of self-expanding and balloon-expandable transcatheter aortic valves morphology and association with paravalvular regurgitation: Evaluation using multidetector computed tomography.

OBJECTIVES: Compare final morphology of self-expanding and balloon-expandable prosthesis and association with paravalvular regurgitation (PVR). BACKGROUND: PVR after transcatheter aortic valve replacement (TAVR) remains a frequent complication. A better understanding of the prosthesis geometry may be important to improve selection of the best device for each case and possibly reduce the rates of PVR. METHODS: Retrospective study including patients consecutively submitted to transcatheter aortic valve replacement: August/2007-October/2016. Three months after the procedure a multidetector computed tomography (MDCT) was performed to assess prosthesis geometry: dimensions, eccentricity, and expansion. RESULTS: A total of 147 individuals were included (mean age of 78.8 ± 6.7 and 50.3% males), 57% treated with a self-expanding prosthesis. On the postprocedure MDCT, the self-expanding group had higher eccentricity index (15.0 vs. 7.1%, p < .001) and lower expansion (68.3 vs. 82.8%, p < .001). In that group, the volume of calcium of landing zone had a significant correlation with eccentricity index and under-expansion. Patients with ≥mild PVR presented higher eccentricity (12.6 vs. 7.9%, p < .001) and lower expansion (68 vs. 75%, p = .012). Eccentricity index and landing zone calcium volume were independent predictors of PVR. CONCLUSIONS: Self-expanding prosthesis have greater eccentricity and under-expansion. Calcium burden exerts more influence in the final morphology of that type of valve. Calcification and eccentricity are associated with the development of PVR. These factors should be considered in the selection of the most appropriate type of prosthesis for each scenario.

TNF induces neutrophil adhesion via formin-dependent cytoskeletal reorganization and activation of ß-integrin function.

Although essential for inflammatory responses, leukocyte recruitment to blood vessel walls in response to inflammatory stimuli, such as TNF-α, can contribute to vascular occlusion in inflammatory diseases, including atherosclerosis. We aimed to further characterize the mechanisms by which TNF stimulates adhesive and morphologic alterations in neutrophils. Microfluidic and intravital assays confirmed the potent effect that TNF has on human and murine neutrophil adhesion and recruitment in vitro and in vivo, respectively. Inhibition of actin polymerization by cytochalasin D significantly diminished TNF-induced human neutrophil adhesion in vitro and abolished TNF-induced membrane alterations and cell spreading. In contrast, TNF-induced increases in ß2-integrin (Mac-1 and LFA-1) expression was not significantly altered by actin polymerization inhibition. Consistent with a role for cytoskeletal rearrangements in TNF-induced adhesion, TNF augmented the activity of the Rho GTPase, RhoA, in human neutrophils. However, inhibition of the major RhoA effector protein, Rho kinase (ROCK), by Y-27632 failed to inhibit TNF-induced neutrophil adhesion. In contrast, the formin FH2 domain inhibitor, SMIFH2, abolished TNF-induced human neutrophil adhesion and diminished leukocyte recruitment in vivo. SMIFH2 also inhibited TNF-induced cytoskeletal reorganization in human neutrophils and abolished the alterations in ß2-integrin expression elicited by TNF stimulation. As such, Rho GTPase/mDia formin-mediated cytoskeletal reorganization appears to participate in the orchestration of TNF-induced neutrophil-adhesive interactions, possibly mediated by formin-mediated actin nucleation and subsequent modulation of ß2-integrin activity on the neutrophil surface. This pathway may represent a pharmacologic target for reducing leukocyte recruitment in inflammatory diseases.

Gender differences in the association of epicardial adipose tissue and coronary artery calcification: EPICHEART study: EAT and coronary calcification by gender.

BACKGROUND: The association of epicardial adipose tissue (EAT) and coronary artery calcification (CAC) seems to differ by gender. However, few studies have controlled for body size, and the ideal method for body size indexing has not been explored. OBJECTIVES: To analyse the effect of gender related-body size and-body fat differences on the association of EAT with CAC. METHODS: This was a prospective cohort of 371 severe aortic stenosis patients (77±8.5year-old, 51% females) referred to cardiac surgery. Agatston calcium score, EAT volume and visceral abdominal fat (VAF) were obtained by computed tomography. Body composition was determined using bioelectrical impedance analysis. Body weight and height were measured to derive body mass index (BMI), body surface area (BSA), and body surface index (BSI). EAT volume was normalized for BSA, weight and height. RESULTS: Median CAC score was higher in men (887; IQR: 2010) than in women (279: IQR: 145) (p<0.01). Similarly, men had higher volume of EAT than women (137±65.6 vs. 106±65.6mL, p<0.01), even when BSA- or height-indexed, but not if weight-indexed. EAT volume was associated with CAC adjusting for adiposity (BMI or BSI and VAF, or fat mass), but not with further adjustment for gender. In a stratified analysis, absolute- and indexed-volumes of EAT were independently associated with CAC in men while no association was found in women (gender-interaction p<0.05). CONCLUSIONS: In these high-risk patients, we demonstrated that EAT was associated with CAC score irrespective of body size, body fat and cardiovascular risk factors in men but not in women.

Association of body mass index and visceral fat with aortic valve calcification and mortality after transcatheter aortic valve replacement: the obesity paradox in severe aortic stenosis.

BACKGROUND: Previous studies showed that metabolic syndrome is associated with aortic valve calcification (AVC) and poor outcomes in aortic stenosis (AS). However, if these associations change and how body fat impacts the prognosis of patients in late stage of the disease have been not yet explored. AIMS: To determine the association of body mass index (BMI) and visceral fat with AVC and mortality after transcatheter aortic valve replacement (TAVR). METHODS: This was a prospective cohort of 170 severe AS patients referred to TAVR. We quantified AVC mass score and fat depots including epicardial adipose tissue, intrathoracic fat, and abdominal visceral (VAF) and subcutaneous fats by computed tomography. Fat depots were indexed to body surface area. All-cause and cardiovascular-related deaths after TAVR were recorded over a median follow-up of 1.2 years. RESULTS: Higher AVC mass was independently associated with low BMI and low VAF. All-cause mortality risk increased with the decrease of BMI and increment of VAF. A stratified analysis by obesity showed that in non-obese, VAF was inversely associated with mortality, whereas in obese, high VAF was associated with higher mortality (p value for interaction < 0.05). At long-term, hazard ratio [HR] with non-obese/low VAF was 2.3 (95% confidence interval [CI] 1.1-4.9; p = 0.021) and HR with obese/high VAF was 2.5 (95% CI 1.1-5.8; p = 0.031) compared with obese/low VAF patients. CONCLUSIONS: In AS patients submitted to TAVR, BMI and VAF were inversely associated with AVC. Pre-intervention assessment of VAF by computed tomography may provide a better discrimination of mortality than BMI alone.

Association between implantation depth assessed by computed tomography and new-onset conduction disturbances after transcatheter aortic valve implantation.

BACKGROUND: Transcatheter aortic valve replacement (TAVR) is often associated with intraventricular conduction disturbances. We aimed to determine the association between implantation depth assessed by multidetector computed tomography (MDCT) and new-onset conduction abnormalities after TAVR. METHODS: Retrospective single-center study including patients consecutively submitted to TAVR, between August/2007 and October/2016, who underwent routine MDCT 3 months after the procedure. The endpoint of conduction disturbances included permanent pacemaker implantation and/or new-onset left bundle-branch block. Implantation depth was determined as the distance between the ventricular end of the prothesis and the native ring, at the level of the non-coronary cusp. RESULTS: 138 patients were included (female gender 52.2%, mean age 78.7 ± 6.9 years). The EuroSCORE II was 4.0 ± 3.9% and 57.2% were treated with self-expanding prosthesis. The endpoint of conduction abnormalities was found in 45.7% (n = 63). The implantation depth was greater in the group with conduction disturbances (7.7 vs 6.4 mm, p = 0.006). Chronic obstructive pulmonary disease, oversizing and implantation depth were independent predictors of conduction abnormalities. Implantation depth had an AUC of 0.64 (p = 0.004) for the prediction of conduction abnormalities and a cut-off value of 7.1 mm predicted the composed endpoint with a sensitivity and specificity of 65% and 70%, respectively. CONCLUSIONS: Implantation depth assessed by MDCT is associated with new-onset conduction disturbances after TAVR. In patients with conduction abnormalities, which do not qualify for the immediate implantation of pacemaker, the assessment of implantation depth by MDCT may be an additional marker of risk to aid decision-making.