JOSE EDUARDO KRIEGER

(Fonte: Lattes)
Índice h a partir de 2011
36
Lattes
ResearcherID
ORCID
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Cardio-Pneumologia, Faculdade de Medicina - Docente
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina
LIM/13 - Laboratório de Genética e Cardiologia Molecular, Hospital das Clínicas, Faculdade de Medicina - Líder

Filtros

Mostrar mais
Limpar filtros

Configurações

search.filters.applied.f.dateIssued: 2021 ×

Resultados de Busca

Agora exibindo 1 - 10 de 21
  • article 18 Citação(ões) na Scopus
    Focal adhesion signaling: Vascular smooth muscle cell contractility beyond calcium mechanisms
    (2021) RIBEIRO-SILVA, J. C.; MIYAKAWA, A. A.; KRIEGER, J. E.
    Smooth muscle cell (SMC) contractility is essential to vessel tone maintenance and blood pressure regulation. In response to vasoconstrictors, calcium-dependent mechanisms promote the activation of the regulatory myosin light chain, leading to increased cytoskeleton tension that favors cell shortening. In contrast, SMC maintain an intrinsic level of a contractile force independent of vasoconstrictor stimulation and sustained SMC contraction beyond the timescale of calcium-dependent mechanisms suggesting the involvement of additional players in the contractile response. Focal adhesions (FAs) are conceivable candidates that may influence SMC contraction. They are required for actin-based traction employed by cells to sense and respond to environmental cues in a process termed mechanotransduction. Depletion of FA proteins impairs SMC contractility, producing arteries that are prone to dissection because of a lack of mechanical stability. Here, we discuss the role of calcium-independent FA signaling mechanisms in SMC contractility. We speculate that FA signaling contributes to the genesis of a variety of SMC phenotypes and discuss the potential implications for mechanical homeostasis in normal and diseased states. ©2021 The Author(s).
  • article 2 Citação(ões) na Scopus
    Variant genotypes associated with reduced expression of RhCE antigens among Brazilian blood donors
    (2021) DEZAN, Marcia Regina; OLIVEIRA, Valeria B.; CONRADO, Marina C. A. V.; ROCHA, Mateus Cardoso da; LUZ, Fabio; GALLUCCI, Antonio; PEREIRA, Alexandre C.; KRIEGER, Jose E.; ROCHA, Vanderson; MENDRONE-JUNIOR, Alfredo; DINARDO, Carla Luana
    Background The genetic diversity of the RHCE gene locus has been explored in diverse populations of different racial backgrounds. Data referring to the diversity of RHCE encoding weakened expression of C, c, E, and e in multiethnic populations is still incomplete. Methods Samples from Brazilian blood donors presenting reduced expression of C, c, E, or e on gel method were selected for the study. All exons and flanking introns of RHCE were genotyped though direct Sanger sequencing for the included donors. Results Sixty-six donors were included: 23 with weak C, 22 with weak c, 6 with weak E, 14 with weak e, and 1 with weak c and E. Among the samples with weak C, the following altered RH*C were encountered: RHCE*CeMA (n = 3), RHCE*Ce941C (n = 1), and RHCE*CeVA (n = 1). RHD*D-CE(4-7)-D was detected in six cases, RHCE*CE was presumably present in five cases, and seven cases were unexplained. Two altered alleles underlay the weak c phenotype: RHCE*ceJAL (n = 20) and RHCE*ce340T (n = 2), and two altered RHCE justified weak e: RHCE*ceMO (n = 6) and RHCE*ceJAL (n = 8). Three variant RHCE were associated with weak E: RHCE*cEJU (n = 4), RHCE*cE382C (n = 1), and RHCE*cEIV (n = 1). The RHCE*cE905A justified one case of weak c and E. Conclusion We describe the distribution of RHCE variants found in association with weak expression of C, c, E, and e in blood donors of multiethnic origin, which differs in comparison to that previously reported for people of African or Caucasian descent.
  • conferenceObject
    Automated radiographic bone suppression with deep convolutional neural networks
    (2021) CARDENAS, Diego Armando Cardona; FERREIRA JUNIOR, Jose Raniery; MORENO, Ramon Alfredo; REBELO, Marina de Fatima de Sa; KRIEGER, Jose Eduardo; GUTIERREZ, Marco Antonio
    Dual-energy subtraction (DES) is a technique that separates soft tissue from bones in a chest radiograph (CR). As DES requires specialized equipment, we propose an automatic method based on convolutional neural networks (CNNs) to generate virtual soft tissue images. A dataset comprising 35 pairs of CR and its soft-tissue version split in training (28 image pairs) and testing (7 image pairs) sets were used with data augmentation. We tested two types of images: the lung region's cropped image and the segmented lung image. The ribs suppression was treated as a local problem, so each image was divided into 784 patches. The U-Net architecture was used to perform bone suppression. We tested two types of loss functions: mean squared error (L-mse) and L-sm, which combines L-mse with the structural similarity index measure (SSIM). Due to the patches overlapping, it was necessary to interpolate the gray levels on the reconstructed image from the predicted patches. Evaluations were based on SSIM and root mean square error (RMSE) over the reconstructed lung area. The combination that presented the best results used the loss L-sm and the segmented lung image as input to the U-Net (SSIM of 0.858 and RMSE of 0.033). We observed that the U-Net has poor performance when trained with cropped images containing all information from the chest cavity and how the loss using local information can improve CR rib bone suppression. Our results suggest that it is possible removing the rib bones accurately in CR using CNN and a patch-based approach.y
  • article 16 Citação(ões) na Scopus
    High stretch induces endothelial dysfunction accompanied by oxidative stress and actin remodeling in human saphenous vein endothelial cells
    (2021) GIRAO-SILVA, T.; FONSECA-ALANIZ, M. H.; RIBEIRO-SILVA, J. C.; LEE, J.; PATIL, N. P.; DALLAN, L. A.; BAKER, A. B.; HARMSEN, M. C.; KRIEGER, J. E.; MIYAKAWA, A. A.
    The rate of the remodeling of the arterialized saphenous vein conduit limits the outcomes of coronary artery bypass graft surgery (CABG), which may be influenced by endothelial dysfunction. We tested the hypothesis that high stretch (HS) induces human saphenous vein endothelial cell (hSVEC) dysfunction and examined candidate underlying mechanisms. Our results showed that in vitro HS reduces NO bioavailability, increases inflammatory adhesion molecule expression (E-selectin and VCAM1) and THP-1 cell adhesion. HS decreases F-actin in hSVECs, but not in human arterial endothelial cells, and is accompanied by G-actin and cofilin's nuclear shuttling and increased reactive oxidative species (ROS). Pre-treatment with the broad-acting antioxidant N-acetylcysteine (NAC) supported this observation and diminished stretch-induced actin remodeling and inflammatory adhesive molecule expression. Altogether, we provide evidence that increased oxidative stress and actin cytoskeleton remodeling play a role in HS-induced saphenous vein endothelial cell dysfunction, which may contribute to predisposing saphenous vein graft to failure.
  • article 2 Citação(ões) na Scopus
    Multi-ancestry genome-wide association study accounting for gene-psychosocial factor interactions identifies novel loci for blood pressure traits
    (2021) SUN, D.; RICHARD, M. A.; MUSANI, S. K.; SUNG, Y. J.; WINKLER, T. W.; SCHWANDER, K.; CHAI, J. F.; GUO, X.; KILPELäINEN, T. O.; VOJINOVIC, D.; ASCHARD, H.; HORTA, B. L.; LIU, C.-T.; BIELAK, L. F.; MOOK-KANAMORI, D. O.; MORRISON, A. C.; PEREIRA, A. C.; PSATY, B. M.; AMIN, N.; FOX, E. R.; KOOPERBERG, C.; WEN, W.; SIM, X.; BIERUT, L.; ROTTER, J. I.; BROWN, M. R.; KARDIA, S. L. R.; FRANCESCHINI, N.; RAO, D. C.; FORNAGE, M.; Lifelines Cohort Study; CHITRALA, K.; YANEK, L. R.; HARTWIG, F. P.; HORIMOTO, A. R. V. R.; LIU, Y.; MANNING, A. K.; NOORDAM, R.; SMITH, A. V.; HARRIS, S. E.; KüHNEL, B.; LYYTIKäINEN, L.-P.; NOLTE, I. M.; ARKING, D. E.; RAURAMAA, R.; MOST, P. J. van der; WANG, R.; WARE, E. B.; WEISS, S.; ARNETT, D. K.; BARAC, A.; BOERWINKLE, E.; BROECKEL, U.; CHAKRAVARTI, A.; CHEN, Y.-D. I.; CUPPLES, L. A.; LUIK, A. I.; DAVIGULUS, M. L.; FUENTES, L. de las; MUTSERT, R. de; VRIES, P. S. de; DELANEY, J. A. C.; ROUX, A. V. Diez; DöRR, M.; FAUL, J. D.; FRETTS, A. M.; GALLO, L. C.; MARTIN, L. W.; GRABE, H. J.; GU, C. C.; HARRIS, T. B.; HARTMAN, C. C. A.; HEIKKINEN, S.; IKRAM, M. A.; ISASI, C.; JOHNSON, W. C.; JONAS, J. B.; KAPLAN, R. C.; MEITINGER, T.; KOMULAINEN, P.; KRIEGER, J. E.; LEVY, D.; LIU, J.; LOHMAN, K.; MILANESCHI, Y.; O'CONNELL, J. R.; PALMAS, W. R.; PETERS, A.; PEYSER, P. A.; PULKKI-RåBACK, L.; RAFFEL, L. J.; ZHAO, W.; REINER, A. P.; RICE, K.; ROBINSON, J. G.; ROSENDAAL, F. R.; SCHMIDT, C. O.; SCHREINER, P. J.; SCHWETTMANN, L.; SHIKANY, J. M.; SHU, X.-O.; SIDNEY, S.; ZHU, X.; SIMS, M.; SMITH, J. A.; SOTOODEHNIA, N.; STRAUCH, K.; TAI, E. S.; TAYLOR, K. D.; UITTERLINDEN, A. G.; DUIJN, C. M. van; WALDENBERGER, M.; WEE, H.-L.; ZONDERMAN, A. B.; WEI, W.-B.; WILSON, G.; XUAN, D.; YAO, J.; ZENG, D.; BECKER, D. M.; DEARY, I. J.; GIEGER, C.; LAKKA, T. A.; LEHTIMäKI, T.; NORTH, K. E.; OLDEHINKEL, A. J.; BARTZ, T. M.; PENNINX, B. W. J. H.; SNIEDER, H.; WANG, Y.-X.; WEIR, D. R.; ZHENG, W.; EVANS, M. K.; GAUDERMAN, W. J.; GUDNASON, V.
    Psychological and social factors are known to influence blood pressure (BP) and risk of hypertension and associated cardiovascular diseases. To identify novel BP loci, we carried out genome-wide association meta-analyses of systolic, diastolic, pulse, and mean arterial BP, taking into account the interaction effects of genetic variants with three psychosocial factors: depressive symptoms, anxiety symptoms, and social support. Analyses were performed using a two-stage design in a sample of up to 128,894 adults from five ancestry groups. In the combined meta-analyses of stages 1 and 2, we identified 59 loci (p value < 5e−8), including nine novel BP loci. The novel associations were observed mostly with pulse pressure, with fewer observed with mean arterial pressure. Five novel loci were identified in African ancestry, and all but one showed patterns of interaction with at least one psychosocial factor. Functional annotation of the novel loci supports a major role for genes implicated in the immune response (PLCL2), synaptic function and neurotransmission (LIN7A and PFIA2), as well as genes previously implicated in neuropsychiatric or stress-related disorders (FSTL5 and CHODL). These findings underscore the importance of considering psychological and social factors in gene discovery for BP, especially in non-European populations. © 2020 The Author(s)
  • article 14 Citação(ões) na Scopus
    Multi-ancestry genome-wide gene-sleep interactions identify novel loci for blood pressure
    (2021) WANG, Heming; NOORDAM, Raymond; CADE, Brian E.; SCHWANDER, Karen; WINKLER, Thomas W.; LEE, Jiwon; SUNG, Yun Ju; BENTLEY, Amy R.; MANNING, Alisa K.; ASCHARD, Hugues; KILPELAINEN, Tuomas O.; ILKOV, Marjan; BROWN, Michael R.; HORIMOTO, Andrea R.; RICHARD, Melissa; BARTZ, Traci M.; VOJINOVIC, Dina; LIM, Elise; NIERENBERG, Jovia L.; LIU, Yongmei; CHITRALA, Kumaraswamynaidu; RANKINEN, Tuomo; MUSANI, Solomon K.; FRANCESCHINI, Nora; RAURAMAA, Rainer; ALVER, Maris; ZEE, Phyllis C.; HARRIS, Sarah E.; MOST, Peter J. van Der; NOLTE, Ilja M.; MUNROE, Patricia B.; PALMER, Nicholette D.; KUHNEL, Brigitte; WEISS, Stefan; WEN, Wanqing; HALL, Kelly A.; LYYTIKAINEN, Leo-Pekka; CONNELL, Jeff O.; EIRIKSDOTTIR, Gudny; LAUNER, Lenore J.; VRIES, Paul S. de; ARKING, Dan E.; CHEN, Han; BOERWINKLE, Eric; KRIEGER, Jose E.; SCHREINER, Pamela J.; SIDNEY, Stephen; SHIKANY, James M.; RICE, Kenneth; CHEN, Yii-Der Ida; GHARIB, Sina A.; BIS, Joshua C.; I, Annemarie Luik; IKRAM, M. Arfan; UITTERLINDEN, Andre G.; AMIN, Najaf; XU, Hanfei; LEVY, Daniel; HE, Jiang; LOHMAN, Kurt K.; ZONDERMAN, Alan B.; RICE, Treva K.; SIMS, Mario; WILSON, Gregory; SOFER, Tamar; RICH, Stephen S.; PALMAS, Walter; YAO, Jie; GUO, Xiuqing; I, Jerome Rotter; BIERMASZ, Nienke R.; MOOK-KANAMORI, Dennis O.; MARTIN, Lisa W.; BARAC, Ana; WALLACE, Robert B.; GOTTLIEB, Daniel J.; KOMULAINEN, Pirjo; HEIKKINEN, Sami; MAGI, Reedik; MILANI, Lili; METSPALU, Andres; STARR, John M.; MILANESCHI, Yuri; WAKEN, R. J.; GAO, Chuan; WALDENBERGER, Melanie; PETERS, Annette; STRAUCH, Konstantin; MEITINGER, Thomas; ROENNEBERG, Till; VOLKER, Uwe; DORR, Marcus; SHU, Xiao-Ou; MUKHERJEE, Sutapa; HILLMAN, David R.; KAHONEN, Mika; WAGENKNECHT, Lynne E.; GIEGER, Christian; GRABE, Hans J.; ZHENG, Wei; PALMER, Lyle J.; LEHTIMAKI, Terho; GUDNASON, Vilmundur; MORRISON, Alanna C.; PEREIRA, Alexandre C.; FORNAGE, Myriam; PSATY, Bruce M.; DUIJN, Cornelia M. van; LIU, Ching-Ti; KELLY, Tanika N.; EVANS, Michele K.; BOUCHARD, Claude; FOX, Ervin R.; KOOPERBERG, Charles; ZHU, Xiaofeng; LAKKA, Timo A.; ESKO, Tonu; NORTH, Kari E.; DEARY, Ian J.; SNIEDER, Harold; PENNINX, Brenda W. J. H.; GAUDERMAN, W. James; RAO, Dabeeru C.; REDLINE, Susan; HEEMST, Diana van
    Long and short sleep duration are associated with elevated blood pressure (BP), possibly through effects on molecular pathways that influence neuroendocrine and vascular systems. To gain new insights into the genetic basis of sleep-related BP variation, we performed genome-wide gene by short or long sleep duration interaction analyses on four BP traits (systolic BP, diastolic BP, mean arterial pressure, and pulse pressure) across five ancestry groups in two stages using 2 degree of freedom (df) joint test followed by 1df test of interaction effects. Primary multi-ancestry analysis in 62,969 individuals in stage 1 identified three novel gene by sleep interactions that were replicated in an additional 59,296 individuals in stage 2 (stage 1 + 2 P-joint < 5 x 10(-8)), including rs7955964 (FIGNL2/ANKRD33) that increases BP among long sleepers, and rs73493041 (SNORA26/C9orf170) and rs10406644 (KCTD15/LSM14A) that increase BP among short sleepers (P-int < 5 x 10(-8)). Secondary ancestry-specific analysis identified another novel gene by long sleep interaction at rs111887471 (TRPC3/KIAA1109) in individuals of African ancestry (P-int = 2 x 10(-6)). Combined stage 1 and 2 analyses additionally identified significant gene by long sleep interactions at 10 loci including MKLN1 and RGL3/ELAVL3 previously associated with BP, and significant gene by short sleep interactions at 10 loci including C2orf43 previously associated with BP (P-int < 10(-3)). 2df test also identified novel loci for BP after modeling sleep that has known functions in sleep-wake regulation, nervous and cardiometabolic systems. This study indicates that sleep and primary mechanisms regulating BP may interact to elevate BP level, suggesting novel insights into sleep-related BP regulation.
  • conferenceObject
    A general fully automated deep-learning method to detect cardiomegaly in chest x-rays
    (2021) FERREIRA-JUNIOR, Jose Raniery; CARDENAS, Diego Armando Cardona; MORENO, Ramon Alfredo; REBELO, Marina de Fdtima de Sa; KRIEGER, Jose Eduardo; GUTIERREZ, Marco Antonio
    Cardiomegaly is a medical condition that leads to an increase in cardiac size. It can be manually assessed using the cardiothoracic ratio from chest x-rays (CXRs). However, as that task can be challenging in such limited examinations, we propose the fully automated cardiomegaly detection in CXR. For this, we first trained convolutional networks (ConvNets) to classify the CXR as positive or negative to cardiomegaly and then evaluated the generalization potential of the trained ConvNets on independent cohorts. This work used frontal CXR images from a public dataset for training/testing and another public and one private dataset to test the models' generalization externally. Training and testing were performed using images cropped with a previously developed U-Net model. Experiments were performed with five topologically different ConvNets, data augmentation techniques, and a 50-50 class-weighing strategy to improve performance and reduce the possibility of bias to the majority class. The receiver operating characteristic curve assessed the performance of the models. DenseNet yielded the highest area under the curve (AUC) on testing (0.818) and external validation (0.809) datasets. Moreover, DenseNet obtained the highest sensitivity overall, yielding up to 0.971 on the private dataset with patients from our hospital. Therefore, DenseNet had a statistically higher potential to identify cardiomegaly. The proposed models, especially those trained with DenseNet convolutional core, automatically detected cardiomegaly with high sensitivity. To the best of our knowledge, this was the first work to design a novel general model for classifying specific deep-learning patterns of cardiomegaly in CXRs.
  • article 0 Citação(ões) na Scopus
    High-volume endurance exercise training stimulates hematopoiesis by increasing ACE NH2-terminal activity
    (2021) MAGALHAES, Flavio de Castro; FERNANDES, Tiago; BASSANEZE, Vinicius; MATTOS, Katt Coelho; SCHETTERT, Isolmar; MARQUES, Fabio Luiz Navarro; KRIEGER, Jose Eduardo; NAVA, Roberto; BARAUNA, Valerio Garrone; OLIVEIRA, Edilamar Menezes de
    One of the health benefits of endurance exercise training (ET) is the stimulation of hematopoiesis. However, the mechanisms underlying ET-induced hematopoietic adaptations are understudied. N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) inhibits proliferation of early hematopoietic progenitor cells. The angiotensin I-converting enzyme (ACE) NH2-terminal promotes hematopoiesis by inhibiting the anti-hematopoietic effect of Ac-SDKP. Here we demonstrate for the first time the role of ACE NH2-terminal in ET-induced hematopoietic adaptations. Wistar rats were subjected to 10 weeks of moderate-(T1) and high-(T2) volume swimming-training. Although both protocols induced classical ET-associated adaptations, only T2 increased plasma ACE NH2-domain activity (by 40%, P=0.0003) and reduced Ac-SDKP levels (by 50%, P<0.0001). T2 increased the number of hematopoietic stem cells (HSCs; similar to 200%, P=0.0008), early erythroid progenitor colonies (similar to 300%, P<0.0001) and reticulocytes (similar to 500%, P=0.0007), and reduced erythrocyte lifespan (similar to 50%, P=0.022). Following, Wistar rats were subjected to T2 or T2 combined with ACE NH2-terminal inhibition (captopril (Cap) treatment: 10 mg.kg(-1).day(-1)). T2 combined with ACE NH2-terminal inhibition prevented Ac-SDKP decrease and attenuated ET-induced hematopoietic adaptations. Altogether, our findings show that ET-induced hematopoiesis was at least partially associated with increased ACE NH2-terminal activity and reduction in the hematopoietic inhibitor Ac-SDKP.
  • article 15 Citação(ões) na Scopus
    Dynamic Crosstalk between Vascular Smooth Muscle Cells and the Aged Extracellular Matrix
    (2021) RIBEIRO-SILVA, Joao Carlos; NOLASCO, Patricia; KRIEGER, Jose Eduardo; MIYAKAWA, Ayumi Aurea
    Vascular aging is accompanied by the fragmentation of elastic fibers and collagen deposition, leading to reduced distensibility and increased vascular stiffness. A rigid artery facilitates elastin to degradation by MMPs, exposing vascular cells to greater mechanical stress and triggering signaling mechanisms that only exacerbate aging, creating a self-sustaining inflammatory environment that also promotes vascular calcification. In this review, we highlight the role of crosstalk between smooth muscle cells and the vascular extracellular matrix (ECM) and how aging promotes smooth muscle cell phenotypes that ultimately lead to mechanical impairment of aging arteries. Understanding the underlying mechanisms and the role of associated changes in ECM during aging may contribute to new approaches to prevent or delay arterial aging and the onset of cardiovascular diseases.
  • article 15 Citação(ões) na Scopus
    Novel Chest Radiographic Biomarkers for COVID-19 Using Radiomic Features Associated with Diagnostics and Outcomes
    (2021) FERREIRA JUNIOR, Jose Raniery; CARDENAS, Diego Armando Cardona; MORENO, Ramon Alfredo; REBELO, Marina de Fatima de Sa; KRIEGER, Jose Eduardo; GUTIERREZ, Marco Antonio
    COVID-19 is a highly contagious disease that can cause severe pneumonia. Patients with pneumonia undergo chest X-rays (XR) to assess infiltrates that identify the infection. However, the radiographic characteristics of COVID-19 are similar to the other acute respiratory syndromes, hindering the imaging diagnosis. In this work, we proposed identifying quantitative/radiomic biomarkers for COVID-19 to support XR assessment of acute respiratory diseases. This retrospective study used different cohorts of 227 patients diagnosed with pneumonia; 49 of them had COVID-19. Automatically segmented images were characterized by 558 quantitative features, including gray-level histogram and matrices of co-occurrence, run-length, size zone, dependence, and neighboring gray-tone difference. Higher-order features were also calculated after applying square and wavelet transforms. Mann-Whitney U test assessed the diagnostic performance of the features, and the log-rank test assessed the prognostic value to predict Kaplan-Meier curves of overall and deterioration-free survival. Statistical analysis identified 51 independently validated radiomic features associated with COVID-19. Most of them were wavelet-transformed features; the highest performance was the small dependence matrix feature of ""low gray-level emphasis"" (area under the curve of 0.87, sensitivity of 0.85, p<0.001). Six features presented short-term prognostic value to predict overall and deterioration-free survival. The features of histogram ""mean absolute deviation"" and size zone matrix ""non-uniformity"" yielded the highest differences on Kaplan-Meier curves with a hazard ratio of 3.20 (p<0.05). The radiomic markers showed potential as quantitative measures correlated with the etiologic agent of acute infectious diseases and to stratify short-term risk of COVID-19 patients.