Healthcare professionals’ role in social media public health campaigns: Analysis of spanish pro vaccination campaign on twitter Ivan Herrera-Peco, Beatriz Jiménez-Gómez, Juan José Peña Deudero, Elvira Benitez De Gracia, Carlos Ruiz-Núñez Healthcare Switzerland, 2021 The COVID-19 pandemic has generated a great impact worldwide both on the population health but also on an economic and social level. In this health emergency, a key element has been and still is the need for information, which has become a daily concern for many people. Social media represent powerful tools for searching and gathering health-related information, thus becoming a new place where health authorities need to be present to disseminate information of preventive measures like vaccines against COVID-19, as well as try to block information against these public health measures. The main goal of this study was to analyze the role that healthcare professionals have in Twitter to support the campaign of public institutions on vaccination against COVID-19. To address this study, an analysis of the messages sent on Twitter containing the hashtag #yomevacuno, between 12 December 2020 was developed using the NodeXL software (Social Media Research Foundation, Redwood, CA, USA), focusing on content analysis of tweets and users’ accounts to identify healthcare professionals. The results show that healthcare professionals represent only 11.38% of users, being responsible for 6.35% of impressions generated by the network #yomevacuno. We can observe that traffic information generated by healthcare professionals is not significant in comparison with institutions (p = 0.633), but it is compared to common users (p = 0.0014). The most active healthcare professionals were pharmacists (40.17%), nurses (27.17%), and physicians (12.14%). Their activity (90.43% of messages) was mainly focused on sharing messages generated by other users’ accounts. From original content generated by healthcare professionals, only 78.95% had a favorable storytelling on the vaccine, but without sharing information about vaccines or vaccination. As a conclusion for this study, the participation of healthcare professionals in the dissemination and generation of information within the #yomevacuno communication strategy, led by the Spanish Ministry of Health, has been scarce. We emphasize the need to enhance communication skills in social networks to support public health campaigns through these increasingly important social media.
Antivaccine movement and covid-19 negationism: A content analysis of spanish-written messages on twitter Ivan Herrera-Peco, Beatriz Jiménez-Gómez, Carlos Santiago Romero Magdalena, Juan José Deudero, María García-Puente, Elvira Benítez De Gracia, Carlos Ruiz Núñez Vaccines, 2021 During the COVID-19 pandemic, different conspiracies have risen, with the most dangerous being those focusing on vaccines. Today, there exists a social media movement focused on destroying the credibility of vaccines and trying to convince people to ignore the advice of governments and health organizations on vaccination. Our aim was to analyze a COVID-19 antivaccination message campaign on Twitter that uses Spanish as the main language, to find the key elements in their communication strategy. Twitter data were retrieved from 14 to 28 December using NodeXL software. We analyzed tweets in Spanish, focusing on influential users, most influential tweets, and content analysis of tweets. The results revealed ordinary citizens who ‘offer the truth’ as the most important profile in this network. The content analysis showed antivaccine tweets (31.05%) as the most frequent. The analysis of anti-COVID19 tweets showed that attacks against vaccine safety were the most important (79.87%) but we detected a new kind of message presenting the vaccine as a means of manipulating the human genetic code (8.1%). We concluded that the antivaccine movement and its tenets have great influence in the COVID-19 negationist movement. We observed a new topic in COVID-19 vaccine hoaxes that must be considered in our fight against misinformation.
Multitype Bellman-Harris branching model provides biological predictors of early stages of adult hippocampal neurogenesis Biao Li, Amanda Sierra, Juan Jose Deudero, Fatih Semerci, Andrew Laitman, Marek Kimmel, Mirjana Maletic-Savatic BMC Systems Biology, 2017 BACKGROUND: Adult hippocampal neurogenesis, the process of formation of new neurons, occurs throughout life in the hippocampus. New neurons have been associated with learning and memory as well as mood control, and impaired neurogenesis has been linked to depression, schizophrenia, autism and cognitive decline during aging. Thus, understanding the biological properties of adult neurogenesis has important implications for human health. Computational models of neurogenesis have attempted to derive biologically relevant knowledge, hard to achieve using experimentation. However, the majority of the computational studies have predominantly focused on the late stages of neurogenesis, when newborn neurons integrate into hippocampal circuitry. Little is known about the early stages that regulate proliferation, differentiation, and survival of neural stem cells and their immediate progeny. RESULTS: Here, based on the branching process theory and biological evidence, we developed a computational model that represents the early stage hippocampal neurogenic cascade and allows prediction of the overall efficiency of neurogenesis in both normal and diseased conditions. Using this stochastic model with a simulation program, we derived the equilibrium distribution of cell population and simulated the progression of the neurogenic cascade. Using BrdU pulse-and-chase experiment to label proliferating cells and their progeny in vivo, we quantified labeled newborn cells and fit the model on the experimental data. Our simulation results reveal unknown but meaningful biological parameters, among which the most critical ones are apoptotic rates at different stages of the neurogenic cascade: apoptotic rates reach maximum at the stage of neuroblasts; the probability of neuroprogenitor cell renewal is low; the neuroblast stage has the highest temporal variance within the cell types of the neurogenic cascade, while the apoptotic stage is short. CONCLUSION: At a practical level, the stochastic model and simulation framework we developed will enable us to predict overall efficiency of hippocampal neurogenesis in both normal and diseased conditions. It can also generate predictions of the behavior of the neurogenic system under perturbations such as increase or decrease of apoptosis due to disease or treatment.
Neuronal Hyperactivity Disturbs ATP Microgradients, Impairs Microglial Motility, and Reduces Phagocytic Receptor Expression Triggering Apoptosis/Microglial Phagocytosis Uncoupling Oihane Abiega, Sol Beccari, Irune Diaz-Aparicio, Agnes Nadjar, Sophie Layé, Quentin Leyrolle, Diego Gómez-Nicola, María Domercq, Alberto Pérez-Samartín, Víctor Sánchez-Zafra, Iñaki Paris, Jorge Valero, Julie C. Savage, Chin-Wai Hui, Marie-Ève Tremblay, Juan J. P. Deudero, Amy L. Brewster, Anne E. Anderson, Laura Zaldumbide, Lara Galbarriatu, Ainhoa Marinas, Maria dM. Vivanco, Carlos Matute, Mirjana Maletic-Savatic, Juan M. Encinas, Amanda Sierra Plos Biology, 2016 Phagocytosis is essential to maintain tissue homeostasis in a large number of inflammatory and autoimmune diseases, but its role in the diseased brain is poorly explored. Recent findings suggest that in the adult hippocampal neurogenic niche, where the excess of newborn cells undergo apoptosis in physiological conditions, phagocytosis is efficiently executed by surveillant, ramified microglia. To test whether microglia are efficient phagocytes in the diseased brain as well, we confronted them with a series of apoptotic challenges and discovered a generalized response. When challenged with excitotoxicity in vitro (via the glutamate agonist NMDA) or inflammation in vivo (via systemic administration of bacterial lipopolysaccharides or by omega 3 fatty acid deficient diets), microglia resorted to different strategies to boost their phagocytic efficiency and compensate for the increased number of apoptotic cells, thus maintaining phagocytosis and apoptosis tightly coupled. Unexpectedly, this coupling was chronically lost in a mouse model of mesial temporal lobe epilepsy (MTLE) as well as in hippocampal tissue resected from individuals with MTLE, a major neurological disorder characterized by seizures, excitotoxicity, and inflammation. Importantly, the loss of phagocytosis/apoptosis coupling correlated with the expression of microglial proinflammatory, epileptogenic cytokines, suggesting its contribution to the pathophysiology of epilepsy. The phagocytic blockade resulted from reduced microglial surveillance and apoptotic cell recognition receptor expression and was not directly mediated by signaling through microglial glutamate receptors. Instead, it was related to the disruption of local ATP microgradients caused by the hyperactivity of the hippocampal network, at least in the acute phase of epilepsy. Finally, the uncoupling led to an accumulation of apoptotic newborn cells in the neurogenic niche that was due not to decreased survival but to delayed cell clearance after seizures. These results demonstrate that the efficiency of microglial phagocytosis critically affects the dynamics of apoptosis and urge to routinely assess the microglial phagocytic efficiency in neurodegenerative disorders.
AG490 promotes HIF-1α accumulation by inhibiting its hydroxylation R. Fernandez-Sanchez, S. Berzal, Maria-Dolores Sanchez-Nino, F. Neria, S. Goncalves, O. Calabia, A. Tejedor, M. J. Calzada, C. Caramelo, J. J.P. Deudero, A. Ortiz Current Medicinal Chemistry, 2012 AG490 is a tyrphostin originally described as a Janus Activated Kinase (JAK) 2 inhibitor. AG490 also inhibits epidermal growth factor receptor (EGFR) and guanylyl cyclases (GC). More recently, AG490 was associated with oxidative stress protection in experimental acute kidney injury models. We now show that AG490 is also a strong activator of the Hypoxia Inducible Factor (HIF)-1. Under normoxic conditions HIF-1α is degraded through hydroxylation, von Hippel Lindau protein (VHL)-mediated ubiquitin tagging and proteasomal degradation. AG490 increased HIF-1α protein, but not HIF-1α mRNA levels, dose- and time-dependently in cultured endothelial, vascular smooth muscle and kidney proximal tubular epithelial cells. AG490 increased HIF-1α protein half-life, suggesting that HIF-1α protein accumulation resulted from a decreased degradation. In this regard, AG490 prevented HIF-1α hydroxylation and increased HIF-1α protein levels in human renal carcinoma cells expressing VHL, but did not further increase HIF-1α in VHL negative cells. AG490 did not prevent the proteasomal degradation of other proteins. HIF-1α was not upregulated by dominant negative JAK2constructs, tyrphostin AG9, the EGFR inhibitors erbstatin and genistein, the GC inhibitor Ly83583 or cGMP analogues. Finally, AG490 also increased HIF-1α transcriptional activity evidenced by the increased HIF-1α-dependent VEGF expression. In conclusion, AG490 is a novel HIF-1α activator that increases HIF-1α half-life and protein levels through interference with HIF-1α hydroxylation and VHL-mediated degradation. This action may contribute to the cell and tissue protective effects of AG490.
Aldosterone increases vascular calcification in "in vitro" studies Nefrologia, 2008
Some insight into the vascular endothelial growth factor/erythropoietin relationship [1] Functional Neurology, 2007
Mechanisms of endothelial cell protection by blockade of the JAK2 pathway Fernando Neria, Carlos Caramelo, Héctor Peinado, Francisco R. González-Pacheco, Juan JP. Deudero, Alain J. de Solis, Ruth Fernández-Sánchez, Silvia Peñate, Amparo Cano, Mª Ángeles Castilla American Journal of Physiology Cell Physiology, 2007
Effects of vascular endothelial growth factor (VEGF) and tumor media on endothelial cell activation and survival Investigacion Cardiovascular, 2006
Response to hypoxia. A systemic mechanism based on the control of gene expression Medicina, 2006
Reticulocyte response after immediate withdrawal of recombinant human erythropoietin in chronic hemodialysis patients Nefrologia, 2004
Tumor-induced endothelial cell activation: Role of vascular endothelial growth factor M. Ángeles Castilla, Fernando Neria, Guadalupe Renedo, Daniel S. Pereira, Francisco R. González-Pacheco, Sonsoles Jiménez, Paloma Tramón, J. J. P. Deudero, M. V. Alvarez Arroyo, Susana Yagüe, Carlos Caramelo American Journal of Physiology Cell Physiology, 2004
Papel del factor de crecimiento endotelial vascular (VEGF) en la protección de las células endoteliales Nefrologia, 2004
Role of VEGF in the cellular response to injury Nefrologia, 2003
