Standardized catch rate of cockfish, Callorhinchus callorynchus, in a bottom trawl fishery of Patagonia: Is it possible its use as a predictor of abundance trend?

Resumo Dados de captura por unidade de esforço (CPUE) do peixe-galo Callorhinchus callorynchus foram avaliados para a pesca de arrasto de fundo no Golfo de San Matías (Patagonia, Argentina), durante o período 1986-2011. Os objetivos do trabalho foram identificar quais os fatores relacionados à dinâmica pesqueira que afetam a taxa de captura do peixe-galo e verificar a viabilidade em utilizar dados de CPUEs padronizadas pelos Modelos Lineares Gerais (GLM) e Modelos Lineares Gerais Mistos (GLMMs) como índices de abundância relativa. A tendência anual da taxa de captura indicou um aumento durante o período avaliado. A CPUE nominal e os índices padronizados pelo Delta-GLM e Delta-GLMM apresentaram a mesma tendência anual, com aumentos de 57%, 61.1% e 60.7%, respectivamente. Os modelos LogNormal foram os de melhor ajuste e explicaram 23,5% da variabilidade total dos dados. Ano, mês, profundidade e "hake" CPUE foram os fatores mais explicativos. A análise dos modelos indicou que a taxa de captura do peixe-galo está ligada à falta de distribuição homogênea do esforço de pesca durante os diferentes anos, meses e navios. Este fato esteve relacionado à dinâmica das frotas na busca das espécies alvo. A tendência crescente no aumento das CPUE e descargas em terra estaria indicando a mudança do esforço de pesca direcionado ao peixe-galo na última década.Abstract The catch per unit of effort (CPUE) data of cockfish, Callorhinchus callorynchus, during 1986-2011 was evaluated for the bottom trawl fishery of the San Matías gulf (Patagonia, Argentina). The objective of this work was to detect what are the factors related to fishery dynamic that affect catch rate of cockfish and to assess standardized CPUE by General linear models (GLMs) and General linear mixed models (GLMMs) as a relative abundance index. The annual trend of the catch rate indicated an increase during the evaluated period. The nominal CPUE and the indices standardized by the Delta-GLM and Delta-GLMM showed the same annual trend, with increases of 57%, 61.1% and 60.7%, respectively. The LogNormal models have the best-fit model and explained 23.5% of the total variability. The factors year, month, depth and hake CPUE explained the highest variability. The analysis of the models indicated that the catch rate of cockfish is subject to the lack of an homogeneous distribution of the fishing effort during different years, months and vessels. This was related to the fleet dynamic searching the targets species. The increasing trend of CPUE and landings would be indicating an increase in effort directionality to the cockfish in the last decade

Elastomeric cardiopatch scaffold for myocardial repair and ventricular support

[EN] OBJECTIVES: Prevention of postischaemic ventricular dilatation progressing towards pathological remodelling is necessary to decrease ventricular wall deterioration. Myocardial tissue engineering may play a therapeutic role due to its capacity to replace the extracellular matrix, thereby creating niches for cell homing. In this experimental animal study, a biomimetic cardiopatch was created with elastomeric scaffolds and nanotechnologies. METHODS: In an experimental animal study in 18 sheep, a cardiopatch was created with adipose tissue-derived progenitor cells seeded into an engineered bioimplant consisting of 3-dimensional bioabsorbable polycaprolactone scaffolds filled with a peptide hydrogel (PuraMatrix (TM)). This patch was then transplanted to cover infarcted myocardium. Non-absorbable poly(ethyl) acrylate polymer scaffolds were used as controls. RESULTS: Fifteen sheep were followed with ultrasound scans at 6 months, including echocardiography scans, tissue Doppler and spectral flow analysis and speckle-tracking imaging, which showed a reduction in longitudinal left ventricular deformation in the cardiopatch-treated group. Magnetic resonance imaging (late gadolinium enhancement) showed reduction of infarct size relative to left ventricular mass in the cardiopatch group versus the controls. Histopathological analysis at 6 months showed that the cardiopatch was fully anchored and integrated to the infarct area with minimal fibrosis interface, thereby promoting angiogenesis and migration of adipose tissue-derived progenitor cells to surrounding tissues. CONCLUSIONS: This study shows the feasibility and effectiveness of a cardiopatch grafted onto myocardial infarction scars in an experimental animal model. This treatment decreased fibrosis, limited infarct scar expansion and reduced postischaemic ventricular deformity. A capillary network developed between our scaffold and the heart. The elastomeric cardiopatch seems to have a positive impact on ventricular remodelling and performance in patients with heart failure.The RECATABI Project (Regeneration of Cardiac Tissue Assisted by Bioactive Implants) was financially supported by the 7th Framework Programme (FP7) of the European Commission. Project ID: 229239. Funded under FP7-NMP and the European Regional Development Fund (FEDER Spain).Chachques, JC.; Lila, N.; Soler Botija, C.; Martínez-Ramos, C.; Vallés Lluch, A.; Autret, G.; Perier, M.... (2020). Elastomeric cardiopatch scaffold for myocardial repair and ventricular support. European Journal of Cardio-Thoracic Surgery. 57(3):545-555. https://doi.org/10.1093/ejcts/ezz252S545555573Madonna, R., Van Laake, L. W., Botker, H. E., Davidson, S. M., De Caterina, R., Engel, F. B., … Sluijter, J. P. G. (2019). ESC Working Group on Cellular Biology of the Heart: position paper for Cardiovascular Research: tissue engineering strategies combined with cell therapies for cardiac repair in ischaemic heart disease and heart failure. Cardiovascular Research, 115(3), 488-500. doi:10.1093/cvr/cvz010Nielsen, S. H., Mouton, A. J., DeLeon-Pennell, K. Y., Genovese, F., Karsdal, M., & Lindsey, M. L. (2019). Understanding cardiac extracellular matrix remodeling to develop biomarkers of myocardial infarction outcomes. Matrix Biology, 75-76, 43-57. doi:10.1016/j.matbio.2017.12.001Spinale, F. G., Frangogiannis, N. G., Hinz, B., Holmes, J. W., Kassiri, Z., & Lindsey, M. L. (2016). Crossing Into the Next Frontier of Cardiac Extracellular Matrix Research. Circulation Research, 119(10), 1040-1045. doi:10.1161/circresaha.116.309916Chachques, J. C., Pradas, M. M., Bayes-Genis, A., & Semino, C. (2013). Creating the bioartificial myocardium for cardiac repair: challenges and clinical targets. Expert Review of Cardiovascular Therapy, 11(12), 1701-1711. doi:10.1586/14779072.2013.854165Bayés-Genís, A., Gálvez-Montón, C., & Roura, S. (2016). Cardiac Tissue Engineering. Journal of the American College of Cardiology, 68(7), 724-726. doi:10.1016/j.jacc.2016.05.055Shafy, A., Fink, T., Zachar, V., Lila, N., Carpentier, A., & Chachques, J. C. (2012). Development of cardiac support bioprostheses for ventricular restoration and myocardial regeneration. European Journal of Cardio-Thoracic Surgery, 43(6), 1211-1219. doi:10.1093/ejcts/ezs480Castells-Sala, C., Recha-Sancho, L., Llucià-Valldeperas, A., Soler-Botija, C., Bayes-Genis, A., & Semino, C. E. (2016). Three-Dimensional Cultures of Human Subcutaneous Adipose Tissue-Derived Progenitor Cells Based on RAD16-I Self-Assembling Peptide. Tissue Engineering Part C: Methods, 22(2), 113-124. doi:10.1089/ten.tec.2015.0270Martínez-Ramos, C., Rodríguez-Pérez, E., Garnes, M. P., Chachques, J. C., Moratal, D., Vallés-Lluch, A., & Monleón Pradas, M. (2014). Design and Assembly Procedures for Large-Sized Biohybrid Scaffolds as Patches for Myocardial Infarct. Tissue Engineering Part C: Methods, 20(10), 817-827. doi:10.1089/ten.tec.2013.0489Biswas, M., Sudhakar, S., Nanda, N. C., Buckberg, G., Pradhan, M., Roomi, A. U., … Houle, H. (2013). Two- and Three-Dimensional Speckle Tracking Echocardiography: Clinical Applications and Future Directions. Echocardiography, 30(1), 88-105. doi:10.1111/echo.12079Dorsey, S. M., McGarvey, J. R., Wang, H., Nikou, A., Arama, L., Koomalsingh, K. J., … Burdick, J. A. (2015). MRI evaluation of injectable hyaluronic acid-based hydrogel therapy to limit ventricular remodeling after myocardial infarction. Biomaterials, 69, 65-75. doi:10.1016/j.biomaterials.2015.08.011Chachques, J. C. (2009). Cellular cardiac regenerative therapy in which patients? Expert Review of Cardiovascular Therapy, 7(8), 911-919. doi:10.1586/erc.09.84Chachques, J. (1997). Dynamic cardiomyoplasty: clinical follow-up at 12 years. European Journal of Cardio-Thoracic Surgery, 12(4), 560-568. doi:10.1016/s1010-7940(97)00214-5Varela, C. E., Fan, Y., & Roche, E. T. (2019). Optimizing Epicardial Restraint and Reinforcement Following Myocardial Infarction: Moving Towards Localized, Biomimetic, and Multitherapeutic Options. Biomimetics, 4(1), 7. doi:10.3390/biomimetics4010007Van den Borne, S. W. M., Cleutjens, J. P. M., Hanemaaijer, R., Creemers, E. E., Smits, J. F. M., Daemen, M. J. A. P., & Blankesteijn, W. M. (2009). Increased matrix metalloproteinase-8 and -9 activity in patients with infarct rupture after myocardial infarction. Cardiovascular Pathology, 18(1), 37-43. doi:10.1016/j.carpath.2007.12.012Ducharme, A., Frantz, S., Aikawa, M., Rabkin, E., Lindsey, M., Rohde, L. E., … Lee, R. T. (2000). Targeted deletion of matrix metalloproteinase-9 attenuates left ventricular enlargement and collagen accumulation after experimental myocardial infarction. Journal of Clinical Investigation, 106(1), 55-62. doi:10.1172/jci8768Sieminski, A. L., Semino, C. E., Gong, H., & Kamm, R. D. (2008). Primary sequence of ionic self-assembling peptide gels affects endothelial cell adhesion and capillary morphogenesis. Journal of Biomedical Materials Research Part A, 87A(2), 494-504. doi:10.1002/jbm.a.31785Bagó, J. R., Soler-Botija, C., Casaní, L., Aguilar, E., Alieva, M., Rubio, N., … Blanco, J. (2013). Bioluminescence imaging of cardiomyogenic and vascular differentiation of cardiac and subcutaneous adipose tissue-derived progenitor cells in fibrin patches in a myocardium infarct model. International Journal of Cardiology, 169(4), 288-295. doi:10.1016/j.ijcard.2013.09.013Chachques, J. C., Trainini, J. C., Lago, N., Cortes-Morichetti, M., Schussler, O., & Carpentier, A. (2008). Myocardial Assistance by Grafting a New Bioartificial Upgraded Myocardium (MAGNUM Trial): Clinical Feasibility Study. The Annals of Thoracic Surgery, 85(3), 901-908. doi:10.1016/j.athoracsur.2007.10.052Lee, H., Ahn, S., Bonassar, L. J., & Kim, G. (2012). Cell(MC3T3-E1)-Printed Poly(ϵ-caprolactone)/Alginate Hybrid Scaffolds for Tissue Regeneration. Macromolecular Rapid Communications, 34(2), 142-149. doi:10.1002/marc.201200524Strub, M., Van Bellinghen, X., Fioretti, F., Bornert, F., Benkirane-Jessel, N., Idoux-Gillet, Y., … Clauss, F. (2018). Maxillary Bone Regeneration Based on Nanoreservoirs Functionalizedε-Polycaprolactone Biomembranes in a Mouse Model of Jaw Bone Lesion. BioMed Research International, 2018, 1-12. doi:10.1155/2018/7380389Rohman, G., Huot, S., Vilas-Boas, M., Radu-Bostan, G., Castner, D. G., & Migonney, V. (2015). The grafting of a thin layer of poly(sodium styrene sulfonate) onto poly(ε-caprolactone) surface can enhance fibroblast behavior. 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Implantable cardioverter defibrillator therapy for primary prevention of sudden cardiac death in the real world: Main findings from the French multicentre DAI-PP programme (pilot phase)

This review summarizes the main findings of the French multicentre DAI-PP pilot programme, and discusses the related clinical and research perspectives. This project included retrospectively (2002–2012 period) more than 5000 subjects with structural heart disease who received an implantable cardioverter defibrillator (ICD) for primary prevention of sudden cardiac death, and were followed for a mean period of 3 years. The pilot phase of the DAI-PP programme has provided valuable information on several practical and clinically relevant aspects of primary prevention ICD implantation in the real-world population, which are summarized in this review. This pilot has led to a prospective evaluation that started in May 2018, assessing ICD therapy in primary and secondary prevention in patients with structural and electrical heart diseases, with remote monitoring follow-up using a dedicated platform. This should further enhance our understanding of sudden cardiac death, to eventually optimize the field of preventative actions

Positional clustering improves computational binding site detection and identifies novel cis-regulatory sites in mammalian GABA(A) receptor subunit genes

Understanding transcription factor (TF) mediated control of gene expression remains a major challenge at the interface of computational and experimental biology. Computational techniques predicting TF-binding site specificity are frequently unreliable. On the other hand, comprehensive experimental validation is difficult and time consuming. We introduce a simple strategy that dramatically improves robustness and accuracy of computational binding site prediction. First, we evaluate the rate of recurrence of computational TFBS predictions by commonly used sampling procedures. We find that the vast majority of results are biologically meaningless. However clustering results based on nucleotide position improves predictive power. Additionally, we find that positional clustering increases robustness to long or imperfectly selected input sequences. Positional clustering can also be used as a mechanism to integrate results from multiple sampling approaches for improvements in accuracy over each one alone. Finally, we predict and validate regulatory sequences partially responsible for transcriptional control of the mammalian type A γ-aminobutyric acid receptor (GABA(A)R) subunit genes. Positional clustering is useful for improving computational binding site predictions, with potential application to improving our understanding of mammalian gene expression. In particular, predicted regulatory mechanisms in the mammalian GABA(A)R subunit gene family may open new avenues of research towards understanding this pharmacologically important neurotransmitter receptor system

II Congrés Internacional sobre Traducció : abril 1994 : actes

Machine learning-based approach unravels distinct pathological signatures induced by patient-derived α-synuclein seeds in monkeys. Dopaminergic neuronal cell death, associated with intracellular α-synuclein (α-syn)-rich protein aggregates [termed "Lewy bodies" (LBs)], is a well-established characteristic of Parkinson's disease (PD). Much evidence, accumulated from multiple experimental models, has suggested that α-syn plays a role in PD pathogenesis, not only as a trigger of pathology but also as a mediator of disease progression through pathological spreading. Here, we have used a machine learning-based approach to identify unique signatures of neurodegeneration in monkeys induced by distinct α-syn pathogenic structures derived from patients with PD. Unexpectedly, our results show that, in nonhuman primates, a small amount of singular α-syn aggregates is as toxic as larger amyloid fibrils present in the LBs, thus reinforcing the need for preclinical research in this species. Furthermore, our results provide evidence supporting the true multifactorial nature of PD, as multiple causes can induce a similar outcome regarding dopaminergic neurodegeneratio

Polymer-Based Reconstruction of the Inferior Vena Cava in Rat: Stem Cells or RGD Peptide?

As part of a program targeted at developing a resorbable valved tube for replacement of the right ventricular outflow tract, we compared three biopolymers (polyurethane [PU], polyhydroxyalkanoate (the poly(3-hydroxybutyrate-co-3-hydroxyvalerate-co-4-hydroxyvalerate) [PHBVV]), and polydioxanone [PDO]) and two biofunctionalization techniques (using adipose-derived stem cells [ADSCs] or the arginine-glycine-aspartate [RGD] peptide) in a rat model of partial inferior vena cava (IVC) replacement. Fifty-three Wistar rats first underwent partial replacement of the IVC with an acellular electrospun PDO, PU, or PHBVV patch, and 31 nude rats subsequently underwent the same procedure using a PDO patch biofunctionalized either by ADSC or RGD. Results were assessed both in vitro (proliferation and survival of ADSC seeded onto the different materials) and in vivo by magnetic resonance imaging (MRI), histology, immunohistochemistry [against markers of vascular cells (von Willebrand factor [vWF], smooth muscle actin [SMA]), and macrophages ([ED1 and ED2] immunostaining)], and enzyme-linked immunosorbent assay (ELISA; for the expression of various cytokines and inducible NO synthase). PDO showed the best in vitro properties. Six weeks after implantation, MRI did not detect significant luminal changes in any group. All biopolymers were evenly lined by vWF-positive cells, but only PDO and PHBVV showed a continuous layer of SMA-positive cells at 3 months. PU patches resulted in a marked granulomatous inflammatory reaction. The ADSC and RGD biofunctionalization yielded similar outcomes. These data confirm the good biocompatibility of PDO and support the concept that appropriately peptide-functionalized polymers may be successfully substituted for cell-loaded materials

Heart Rate and Risk of Cancer Death in Healthy Men

BACKGROUND: Data from several previous studies examining heart-rate and cardiovascular risk have hinted at a possible relationship between heart-rate and non-cardiac mortality. We thus systematically examined the predictive value of heart-rate variables on the subsequent risk of death from cancer. METHODS: In the Paris Prospective Study I, 6101 asymptomatic French working men aged 42 to 53 years, free of clinically detectable cardiovascular disease and cancer, underwent a standardized graded exercise test between 1967 and 1972. Resting heart-rate, heart-rate increase during exercise, and decrease during recovery were measured. Change in resting heart-rate over 5 years was also available in 5139 men. Mortality including 758 cancer deaths was assessed over the 25 years of follow-up. FINDINGS: There were strong, graded and significant relationships between all heart-rate parameters and subsequent cancer deaths. After adjustment for age and tobacco consumption and, compared with the lowest quartile, those with the highest quartile for resting heart-rate had a relative risk of 2.4 for cancer deaths (95% confidence interval: 1.9-2.9, p<0.0001) This was similar after adjustment for traditional cardiovascular risk factors and was observed for the commonest malignancies (respiratory and gastrointestinal). Similarly, significant relationships with cancer death were observed between poor heart rate increase during exercise, poor decrease during recovery and greater heart-rate increase over time (p<0.0001 for all). INTERPRETATION: Resting and exercise heart rate had consistent, graded and highly significant associations with subsequent cancer mortality in men

TRPM2-mediated rise in mitochondrial Zn2+ promotes palmitate-induced mitochondrial fission and pancreatic β-cell death in rodents

Rise in plasma free fatty acids (FFAs) represents a major risk factor for obesity-induced type 2 diabetes. Saturated FFAs cause a progressive decline in insulin secretion by promoting pancreatic β-cell death through increased production of reactive oxygen species (ROS). Recent studies have demonstrated that palmitate (a C16-FFA)-induced rise in ROS causes β-cell death by triggering mitochondrial fragmentation, but the underlying mechanisms are unclear. Using the INS1-832/13 β-cell line, here we demonstrate that palmitate generates the ROS required for mitochondrial fission by activating NOX (NADPH oxidase)-2. More importantly, we show that chemical inhibition, RNAi-mediated silencing and knockout of ROS-sensitive TRPM (transient receptor potential melastatin)-2 channels prevent palmitate-induced mitochondrial fission. Although TRPM2 activation affects the intracellular dynamics of Ca2+ and Zn2+, chelation of Zn2+ alone was sufficient to prevent mitochondrial fission. Consistent with the role of Zn2+, palmitate caused a rise in mitochondrial Zn2+, leading to Zn2+-dependent mitochondrial recruitment of Drp-1 (a protein that catalyses mitochondrial fission) and loss of mitochondrial membrane potential. In agreement with the previous reports, Ca2+ caused Drp-1 recruitment, but it failed to induce mitochondrial fission in the absence of Zn2+. These results indicate a novel role for Zn2+ in mitochondrial dynamics. Inhibition or knockout of TRPM2 channels in mouse islets and RNAi-mediated silencing of TRPM2 expression in human islets prevented FFA/cytokine-induced β-cell death, findings that are consistent with the role of abnormal mitochondrial fission in cell death. To conclude, our results reveal a novel, potentially druggable signalling pathway for FFA-induced β-cell death. The cascade involves NOX-2-dependent production of ROS, activation of TRPM2 channels, rise in mitochondrial Zn2+, Drp-1 recruitment and abnormal mitochondrial fission