Miembros del Grupo
Coordinador
Investigadores
Ana
Pardo Saganta
Felipe Luis
Prósper Cardoso (Co-coordinador)
Colaboradores
Gloria María
Abizanda Sarasa
Paula
Barlabé Ginesta
Paula
García Olloqui
Tania
Lopez Montez
Leyre
López Muneta
Rebeca
Martínez Turrillas
Purificación
Ripalda Cemborain
Juan Antonio
Romero Torrecilla
Líneas de Investigación
- Cardiac Regeneration (Regeneración cardíaca)
- Clinical applications of advanced therapies (Aplicaciones clínicas de las terapias avanzadas)
- Pathogenic mechanisms of fibrosis and therapeutics strategies for tissue repair (mecanismos patogénicos de la fibrosis y nuevas estrategias terapéuticas)
- Terapia celular e ingeniería de tejidos en patología osteoarticular
Palabras Clave
- Células madre
- Fibrosis
- Medicamentos de terapias avanzadas
- Reprogramación
- Terapia celular
Publicaciones Científicas desde 2018
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Autores: Paz-Artigas, L.; Montero Calle, Maria del Pilar; Iglesias García, Olalla; et al.Revista: INTERNATIONAL JOURNAL OF PHARMACEUTICSISSN: 0378-5173 Vol.632 2023 págs. 122589ResumenMyocardial ischaemia is one of the leading dead causes worldwide. Although animal experiments have histor-ically provided a wealth of information, animal models are time and money consuming, and they usually miss typical human patient's characteristics associated with ischemia prevalence, including aging and comorbidities. Generating reliable in vitro models that recapitulate the human cardiac microenvironment during an ischaemic event can boost the development of new drugs and therapeutic strategies, as well as our understanding of the underlying cellular and molecular events, helping the optimization of therapeutic approaches prior to animal and clinical testing. Although several culture systems have emerged for the recreation of cardiac physiology, mimicking the features of an ischaemic heart tissue in vitro is challenging and certain aspects of the disease process remain poorly addressed. Here, current in vitro cardiac culture systems used for modelling cardiac ischaemia, from self-aggregated organoids to scaffold-based constructs and heart-on-chip platforms are described. The advantages of these models to recreate ischaemic hallmarks such as oxygen gradients, patho-logical alterations of mechanical strength or fibrotic responses are highlighted. The new models represent a step forward to be considered, but unfortunately, we are far away from recapitulating all complexity of the clinical situations.
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Autores: Pérez Estenaga, Íñigo; Chevalier, M. T.; Pena, E.; et al.Revista: ACS APPLIED MATERIALS AND INTERFACESISSN: 1944-8244 Vol.15 N° 44 2023 págs. 50638 - 50651ResumenIschemic heart diseaseis one of the leading causes ofdeath worldwide.The efficient delivery of therapeutic growth factors could counteractthe adverse prognosis of post-myocardial infarction (post-MI). Inthis study, a collagen hydrogel that is able to load and appropriatelydeliver pro-angiogenic stromal cell-derived factor 1 (SDF1) was physicallycoupled with a compact collagen membrane in order to provide the suturestrength required for surgical implantation. This bilayer collagen-on-collagenscaffold (bCS) showed the suitable physicochemical properties thatare needed for efficient implantation, and the scaffold was able todeliver therapeutic growth factors after MI. In vitro collagen matrix biodegradation led to a sustained SDF1 release anda lack of cytotoxicity in the relevant cell cultures. In vivo intervention in a rat subacute MI model resulted in the full integrationof the scaffold into the heart after implantation and biocompatibilitywith the tissue, with a prevalence of anti-inflammatory and pro-angiogenicmacrophages, as well as evidence of revascularization and improvedcardiac function after 60 days. Moreover, the beneficial effect ofthe released SDF1 on heart remodeling was confirmed by a significantreduction in cardiac tissue stiffness. Our findings demonstrate thatthis multimodal scaffold is a desirable matrix that can be used asa drug delivery system and a scaffolding material to promote functionalrecovery after MI.
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Autores: Romero Torrecilla, Juan Antonio; Lamo de Espinosa Vázquez de Sola, José María; Ripalda Cemborain, Purificación; et al.Revista: NPJ REGENERATIVE MEDICINEISSN: 2057-3995 Vol.8 N° 1 2023 págs. 54ResumenDuring bone regeneration, the periosteum acts as a carrier for key regenerative cues, delivering osteochondroprogenitor cells and crucial growth factors to the injured bone. We developed a biocompatible, 3D polycaprolactone (PCL) melt electro-written membrane to act as a mimetic periosteum. Poly (ethyl acrylate) coating of the PCL membrane allowed functionalization, mediated by fibronectin and low dose recombinant human BMP-2 (rhBMP-2) (10-25 mu g/ml), resulting in efficient, sustained osteoinduction in vitro. In vivo, rhBMP-2 functionalized mimetic periosteum demonstrated regenerative potential in the treatment of rat critical-size femoral defects with highly efficient healing and functional recovery (80%-93%). Mimetic periosteum has also proven to be efficient for cell delivery, as observed through the migration of transplanted periosteum-derived mesenchymal cells to the bone defect and their survival. Ultimately, mimetic periosteum demonstrated its ability to deliver key stem cells and morphogens to an injured site, exposing a therapeutic and translational potential in vivo when combined with unprecedentedly low rhBMP-2 doses.
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Autores: Pérez Mozas, María (Autor de correspondencia); Payo Ollero, Jesús; Montiel Terrón, Veronica; et al.Revista: JOURNAL OF KNEE SURGERYISSN: 1538-8506 Vol.36 N° 1 2023 págs. 79 - 86ResumenThe purpose of this study was to determine if driving ability 6 weeks after anterior cruciate ligament (ACL) reconstruction is affected by the addition of a meniscal suture. It was also hypothesized that no differences in the driving performance would be found between right or left knee surgery subgroups. A total of 82 people participated in this prospective cohort study: 36 healthy controls, 26 patients undergoing isolated ACL (iACL) reconstruction with hamstring autograft, and 20 patients undergoing ACL and meniscal suture (ACL-MS) reconstruction. ACL-MS group followed a weight-bearing and movement restriction protocol during the first 2 postoperative weeks, whereas patients undergoing iACL could start range-of-motion exercises and full weight-bearing ambulation on the first postoperative day. A driving simulator that reproduced real-life driving conditions was used to evaluate driving ability. The software analyzed multiple driving and braking variables. Driving performance in the sixth postoperative week was compared with that of a healthy control group. Subgroup analysis considering additional procedures (iACL, ACL-MS) and the side of the operated knee (right, left) was also performed. No statistically significant differences were found in the demographic characteristics nor in the driving performance (collisions, p =0.897; sidewalk invasions, p =0.749; pedestrian impact, p =0.983) between iACL, ACL-MS, and control groups. No statistically significant differences were found in right-left subgroup analysis. The results of the present study show that patients in their sixth postoperative week after right or left ACL reconstruction showed similar driving performance as compared with a healthy control group, regardless of associating or not a meniscal suture, suggesting it is safe to resume driving 6 weeks after the mentioned surgeries.
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Autores: Moya Jodar, Marta; Ullate Agote, Asier; Barlabe Ginesta, Paula; et al.Revista: STEM CELL REPORTSISSN: 2213-6711 Vol.18 N° 1 2023 págs. 64 - 80ResumenNaive human pluripotent stem cells (hPSCs) are defined as the in vitro counterpart of the human preimplantation embryo's epiblast and are used as a model system to study developmental processes. In this study, we report the discovery and characterization of distinct cell populations coexisting with epiblast-like cells in 5iLAF naive human induced PSC (hiPSC) cultures. It is noteworthy that these populations closely resemble different cell types of the human embryo at early developmental stages. While epiblast-like cells represent the main cell population, interestingly we detect a cell population with gene and transposable element expression profile closely resembling the totipotent eight-cell (8C)-stage human embryo, and three cell populations analogous to trophectoderm cells at different stages of their maturation process: transition, early, and mature stages. Moreover, we reveal the presence of cells resembling primitive endoderm. Thus, 5iLAF naive hiPSC cultures provide an excellent opportunity to model the earliest events of human embryogenesis, from the 8C stage to the peri-implantation period.
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Autores: Spoto, S. (Autor de correspondencia); Argemí Ballbé, José María; Di Costanzo, R. (Autor de correspondencia); et al.Revista: JOURNAL OF PERSONALIZED MEDICINEISSN: 2075-4426 Vol.13 N° 7 2023 págs. 1155ResumenBackground: Acute heart failure (AHF) is a major cause of hospitalization and mortality worldwide. Early and accurate diagnosis, as well as effective risk stratification, are essential for optimizing clinical management and improving patient outcomes. In this context, biomarkers have gained increasing interest in recent years as they can provide important diagnostic and prognostic information in patients with AHF. Aim and Methods: The primary objective of the present study was to compare the levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP), mid-regional pro-adrenomedullin (MR-proADM), and C-reactive protein (CRP) between patients diagnosed with acute heart failure (AHF) and those without AHF and sepsis. Furthermore, the study aimed to assess the diagnostic and prognostic value of the use of a multimarker approach in AHF patients. To achieve these objectives, a total of 145 patients with AHF and 127 patients without AHF and sepsis, serving as the control group, were consecutively enrolled in the study. Results: Levels of MR-proADM (median: 2.07; (25th-75th percentiles: 1.40-3.02) vs. 1.11 (0.83-1.71) nmol/L, p < 0.0001), and NT-proBNP (5319 (1691-11,874) vs. 271 (89-931.5) pg/mL, p < 0.0001) were significantly higher in patients with AHF compared to controls, whereas CRP levels did not show significant differences. The mortality rate in the AHF group during in-hospital stay was 12%, and the rate of new re-admission for AHF within 30 days after discharge was 10%. During in-hospital follow-up, Cox regression analyses showed that levels of NT-proBNP > 10,132 pg/mL (hazard ratio (HR) 2.97; 95% confidence interval (CI): 1.13-7.82; p = 0.0284) and levels of MR-proADM > 2.8 nmol/L (HR: 8.57; CI: 2.42-30.28; p = 0.0009) predicted mortality. The combined use of MR-proADM and NT-proBNP provided significant additive predictive value for mortality and new re-admission for AHF at 30 days after discharge. A logistic regression analysis showed that the presence of NT-proBNP pg/mL > 12,973 pg mL and/or MR-proADM > 4.2 nmol/L predicted hospital re-admission within 30 days (OR: 3.23; CI: 1.05-9.91; p = 0.041). Conclusion: The combined assay of MR-proADM and NT-proBNP could be helpful in accurately identifying AHF and in defining prognosis and re-admission for AHF. The complementary use of these biomarkers can provide a useful clinical evaluation of AHF while also orienting clinicians to the pathophysiology underlying heart damage and assisting them in tailoring therapy.
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Autores: Montero Calle, Maria del Pilar; Flandes Iparraguirre, María; Kuebler, B.; et al.Revista: STEM CELL RESEARCHISSN: 1873-5061 Vol.71 2023 págs. 103189ResumenTransthyretin (TTR) amyloid cardiomyopathy (ATTR-CM) is a life-threatening disease caused by the abnormal production of misfolded TTR protein by liver cells, which is then released systemically. Its amyloid deposition in the heart is linked to cardiac toxicity and progression toward heart failure. A human induced pluripotent stem cell (iPSC) line was generated from peripheral blood mononuclear cells (PBMCs) from a patient suffering familial transthyretin amyloid cardio-myopathy carrying a c.128G>A (p.Ser43Asn) mutation in the TTR gene. This iPSC line offers a useful resource to study the disease pathophysiology and a cell-based model for therapeutic discovery.
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Autores: Ozkan, H.; Di Francesco, M.; Willcockson, H.; et al.Revista: DRUG DELIVERY AND TRANSLATIONAL RESEARCHISSN: 2190-393X Vol.13 N° 2 2023 págs. 689 - 701ResumenPosttraumatic osteoarthritis (PTOA) is mostly treated via corticosteroid administration, and total joint arthroplasty continues to be the sole effective intervention in severe conditions. To assess the therapeutic potential of CCR2 targeting in PTOA, we used biodegradable microplates (mu PLs) to achieve a slow and sustained intraarticular release of the CCR2 inhibitor RS504393 into injured knees and followed joint damage during disease progression. RS504393-loaded mu PLs (RS-mu PLs) were fabricated via a template-replica molding technique. A mixture of poly(lactic-co-glycolic acid) (PLGA) and RS504393 was deposited into 20 x 10 mu m (length x height) wells in a polyvinyl alcohol (PVA) square-patterned template. After physicochemical and toxicological characterizations, the RS504393 release profile from mu PL was assessed in PBS buffer. C57BL/6 J male mice were subjected to destabilization of the medial meniscus (DMM)/sham surgery, and RS-mu PLs (1 mg/kg) were administered intraarticularly 1 week postsurgery. Administrations were repeated at 4 and 7 weeks post-DMM. Drug free-mu PLs (DF-mu PLs) and saline injections were performed as controls. Mice were euthanized at 4 and 10 weeks post-DMM, corresponding to the early and severe PTOA stages, respectively. Knees were evaluated for cartilage structure score (ACS, H&E), matrix loss (safranin O score), osteophyte formation and maturation from cartilage to bone (cartilage quantification), and subchondral plate thickness. The RS-mu PL architecture ensured the sustained release of CCR2 inhibitors over several weeks, with similar to 20% of RS504393 still available at 21 days. This prolonged release improved cartilage structure and reduced bone damage and synovial hyperplasia at both PTOA stages. Extracellular matrix loss was also attenuated, although with less efficacy. The results indicate that local sustained delivery is needed to optimize CCR2-targeted therapies.
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Autores: Flandes Iparraguirre, María; Montero Calle, Maria del Pilar; Iglesias García, Olalla; et al.Revista: TISSUE ENGINEERING PART AISSN: 1937-3341 Vol.29 N° 11-12 2023 págs. 237 - 238
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Autores: Montero Calle, Maria del Pilar; Calatayud-Sanchez, A.; Gavira Gómez, Juan José; et al.Revista: TISSUE ENGINEERING PART AISSN: 1937-3341 Vol.29 N° 11-12 2023 págs. 1377 - 1378
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Autores: Fernández-Santos, M. E. (Autor de correspondencia); García-Arranz, M.; Andreu Oltra, Enrique José; et al.Revista: FRONTIERS IN IMMUNOLOGYISSN: 1664-3224 Vol.13 2022 págs. 918565ResumenMSCs products as well as their derived extracellular vesicles, are currently being explored as advanced biologics in cell-based therapies with high expectations for their clinical use in the next few years. In recent years, various strategies designed for improving the therapeutic potential of mesenchymal stromal cells (MSCs), including pre-conditioning for enhanced cytokine production, improved cell homing and strengthening of immunomodulatory properties, have been developed but the manufacture and handling of these cells for their use as advanced therapy medicinal products (ATMPs) remains insufficiently studied, and available data are mainly related to non-industrial processes. In the present article, we will review this topic, analyzing current information on the specific regulations, the selection of living donors as well as MSCs from different sources (bone marrow, adipose tissue, umbilical cord, etc.), in-process quality controls for ensuring cell efficiency and safety during all stages of the manual and automatic (bioreactors) manufacturing process, including cryopreservation, the use of cell banks, handling medicines, transport systems of ATMPs, among other related aspects, according to European and US legislation. Our aim is to provide a guide for a better, homogeneous manufacturing of therapeutic cellular products with special reference to MSCs.
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Autores: Egea-Zorrilla, A.; Vera Álvarez, Laura; Sáez Ochoa, Borja; et al.Revista: CELLSISSN: 2073-4409 Vol.11 N° 16 2022 págs. 2595ResumenThe lung epithelium is constantly exposed to harmful agents present in the air that we breathe making it highly susceptible to damage. However, in instances of injury to the lung, it exhibits a remarkable capacity to regenerate injured tissue thanks to the presence of distinct stem and progenitor cell populations along the airway and alveolar epithelium. Mechanisms of repair are affected in chronic lung diseases such as idiopathic pulmonary fibrosis (IPF), a progressive life-threatening disorder characterized by the loss of alveolar structures, wherein excessive deposition of extracellular matrix components cause the distortion of tissue architecture that limits lung function and impairs tissue repair. Here, we review the most recent findings of a study of epithelial cells with progenitor behavior that contribute to tissue repair as well as the mechanisms involved in mouse and human lung regeneration. In addition, we describe therapeutic strategies to promote or induce lung regeneration and the cell-based strategies tested in clinical trials for the treatment of IPF. Finally, we discuss the challenges, concerns and limitations of applying these therapies of cell transplantation in IPF patients. Further research is still required to develop successful strategies focused on cell-based therapies to promote lung regeneration to restore lung architecture and function.
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Autores: Antoñanzas Pérez, Javier; Pelacho Samper, Beatriz; Alkorta Aranburu, Gorka; et al.Título: Familial primary cutaneous amyloidosis: caspase activation may be involved in amyloid formationRevista: EXPERIMENTAL DERMATOLOGYISSN: 0906-6705 Vol.31 N° 10 2022 págs. 1638 - 1640
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Autores: Lamo de Espinosa Vázquez de Sola, José María (Autor de correspondencia); Alfonso, A.; Pascual, E.; et al.Revista: DIAGNOSTICSISSN: 2075-4418 Vol.12 N° 5 2022 págs. 1128ResumenObjective: The aim of the study is to describe the morphology associated with the development of osteoarthritis (OA) in three different age groups. These data will contribute to defining the morphology associated with early and late hip OA. Methods: We studied 400 hips in 377 patients who had undergone primary THA due to idiopathic OA. Three groups were compared: group 1 (n = 147), younger patients, aged up to 60 years; group 2 (n = 155), patients aged between 61 and 74 years; and group 3 (n = 98), aged 75 or over. Five independent researchers measured the hip angles and the mean values were used to build a database. Results: No differences between groups in sex distribution and BMI were detected. Less coverage of the head (extrusion index), higher Tonnis angle, lower Wiberg and alpha angles characterized early OA hips. These differences increased with age, being greater between group 2 and group 3 (p < 0.01). However, significant differences were still present in the comparison between group 1 and group 2 (p < 0.01)). No differences were detected between group 2 and group 3. Conclusion: Elevated acetabular angle, head extrusion and decreased Wiberg angle characterize hip osteoarthritis at younger ages and should be the focus of hip preservation surgery in terms of osteoarthritis prevention. Pincer-type FAI (higher Wiberg and lower Tonnis angle) and higher alpha angle (CAM) are correlated with the development of later OA. These results shed doubt on applying the hip preservation surgery concept in terms of osteoarthritis prevention in FAI, especially in Pincer-type FAI patients.
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Autores: Aguado Álvaro, Laura Pilar; Garitano-Larrea, N.; Abizanda Sarasa, Gloria María; et al.Revista: BIOMEDICINESISSN: 2227-9059 Vol.10 N° 10 2022 págs. 2350ResumenSeveral Cre recombinase transgenic mouse models have been generated for cardiac fibroblast (CF) tracking and heart regulation. However, there is still no consensus on the ideal mouse model to optimally identify and/or regulate these cells. Here, a comparative evaluation of the efficiency and specificity of the indirect reporter Cre-loxP system was carried out in three of the most commonly used fibroblast reporter transgenic mice (Pdgfra-CreERT2, Col1a1-CreERT2 and PostnMCM) under healthy and ischemic conditions, to determine their suitability in in vivo studies of cardiac fibrosis. We demonstrate optimal Cre recombinase activity in CF (but also, although moderate, in endothelial cells (ECs)) derived from healthy and infarcted hearts in the PDGFRa-creERT2 mouse strain. In contrast, no positive reporter signal was found in CF derived from the Col1a1-CreERT2 mice. Finally, in the PostnMCM line, fluorescent reporter expression was specifically detected in activated CF but not in EC, which leads us to conclude that it may be the most reliable model for future studies on cardiovascular disease. Importantly, no lethality or cardiac fibrosis were induced after tamoxifen administration at the established doses, either in healthy or infarcted mice of the three fibroblast reporter lineages. This study lays the groundwork for future efficient in vivo CF tracking and functional analyses.
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Autores: Gil-Melgosa, L.; Grasa, J.; Urbiola, A.; et al.Título: Muscular and tendon degeneration after achilles rupture: new insights into future repair strategiesRevista: BIOMEDICINESISSN: 2227-9059 Vol.10 N° 1 2022 págs. 19ResumenAchilles tendon rupture is a frequent injury with an increasing incidence. After clinical surgical repair, aimed at suturing the tendon stumps back into their original position, the repaired Achilles tendon is often plastically deformed and mechanically less strong than the pre-injured tissue, with muscle fatty degeneration contributing to function loss. Despite clinical outcomes, pre-clinical research has mainly focused on tendon structural repair, with a lack of knowledge regarding injury progression from tendon to muscle and its consequences on muscle degenerative/regenerative processes and function. Here, we characterize the morphological changes in the tendon, the myotendinous junction and muscle belly in a mouse model of Achilles tendon complete rupture, finding cellular and fatty infiltration, fibrotic tissue accumulation, muscle stem cell decline and collagen fiber disorganization. We use novel imaging technologies to accurately relate structural alterations in tendon fibers to pathological changes, which further explain the loss of muscle mechanical function after tendon rupture. The treatment of tendon injuries remains a challenge for orthopedics. Thus, the main goal of this study is to bridge the gap between clinicians' knowledge and research to address the underlying pathophysiology of ruptured Achilles tendon and its consequences in the gastrocnemius. Such studies are necessary if current practices in regenerative medicine for Achilles tendon ruptures are to be improved.
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Autores: López Muneta, Leyre; Linares Acosta, Javier; Casis, O.; et al.Revista: FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGYISSN: 2296-634X Vol.9 2022 págs. 797927ResumenDirect cardiac reprogramming has emerged as an interesting approach for the treatment and regeneration of damaged hearts through the direct conversion of fibroblasts into cardiomyocytes or cardiovascular progenitors. However, in studies with human cells, the lack of reporter fibroblasts has hindered the screening of factors and consequently, the development of robust direct cardiac reprogramming protocols.In this study, we have generated functional human NKX2.5(GFP) reporter cardiac fibroblasts. We first established a new NKX2.5(GFP) reporter human induced pluripotent stem cell (hiPSC) line using a CRISPR-Cas9-based knock-in approach in order to preserve function which could alter the biology of the cells. The reporter was found to faithfully track NKX2.5 expressing cells in differentiated NKX2.5(GFP) hiPSC and the potential of NKX2.5-GFP + cells to give rise to the expected cardiac lineages, including functional ventricular- and atrial-like cardiomyocytes, was demonstrated. Then NKX2.5(GFP) cardiac fibroblasts were obtained through directed differentiation, and these showed typical fibroblast-like morphology, a specific marker expression profile and, more importantly, functionality similar to patient-derived cardiac fibroblasts. The advantage of using this approach is that it offers an unlimited supply of cellular models for research in cardiac reprogramming, and since NKX2.5 is expressed not only in cardiomyocytes but also in cardiovascular precursors, the detection of both induced cell types would be possible. These reporter lines will be useful tools for human direct cardiac reprogramming research and progress in this field.
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Autores: Montiel Terrón, Veronica (Autor de correspondencia); Valentí Azcárate, Andrés; Villas Tomé, Carlos; et al.Revista: ARCHIVES OF ORTHOPAEDIC AND TRAUMA SURGERYISSN: 0936-8051 Vol.142 N° 8 2022 págs. 1793 - 1800ResumenPurpose A question still remains as to whether constrictive toe-box shoes (TBS) cause disability only due to pain on pressure points or if they can cause permanent changes in the hallux anatomy. The aim of this study is to compare the hallux morphology in 3 groups classified according to their use of constrictive or open TBS. Methods 424 patients were classified into 3 groups: group A used open TBS daily; group B used constrictive TBS daily; group C used both open and constrictive TBS. Hallux's angles, presence of exostoses and shape of the distal phalanx (DP) were analyzed on dorsoplantar weight-bearing radiographs and compared amongst groups. Results The intermetatarsal (IMA), metatarsophalangeal (MTPA), DASA, PASA, interphalangeal (IPA), obliquity (AP1), asymmetry (AP2) and joint deviation (JDA) angles for group A were 10 degrees, 8 degrees, 5 degrees, 4 degrees, 9 degrees, 3 degrees, 5 degrees, 3 degrees; for group B were 9 degrees, 19 degrees, 5 degrees, 6 degrees, 12 degrees, 2 degrees, 8 degrees, 2 degrees; and for group C were 10 degrees, 10 degrees, 4 degrees, 4 degrees, 12 degrees, 3 degrees, 8 degrees, 1 degrees. Only the differences in the MTPA, IPA and AP2 were statistically significant (p < 0.05). The prevalence of exostoses on the tibial side of the DP was 22, 36, and 29% in groups A, B and C, respectively (p < 0.05). We found similar distributions of the different DP shapes in the three groups. Conclusions Our results suggest that the use of constrictive TBS, even if used only occasionally, could change hallux anatomy from a young age increasing MTPA, IPA and AP2. Moreover, we have found that DP exostoses are present as a "normal variation" in patients who wear an open TBS, but their prevalence is higher in those wearing constrictive toe-box shoes. This could be due to a reactive bone formation secondary to the friction caused by the inner border of the shoe. Level of clinical evidence 3.
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Autores: Urtaza, U. (Autor de correspondencia); Guaresti, O.; Gorronogoitia, I.; et al.Revista: BIOMEDICAL MATERIALSISSN: 1748-6041 Vol.17 N° 4 2022 págs. 045028ResumenThis work identifies and describes different material-scaffold geometry combinations for cartilage tissue engineering (CTE). Previously reported potentially interesting scaffold geometries were tuned and printed using bioresorbable polycaprolactone and poly(lactide-b-ethylene) block copolymer. Medical grades of both polymers were 3D printed with fused filament fabrication technology within an ISO 7 classified cleanroom. Resulting scaffolds were then optically, mechanically and biologically tested. Results indicated that a few material-scaffold geometry combinations present potential for excellent cell viability as well as for an enhance of the chondrogenic properties of the cells, hence suggesting their suitability for CTE applications.
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Autores: Moya Jodar, Marta; Coppiello, Giulia; Rodríguez Madoz, Juan Roberto; et al.Revista: ANIMALSISSN: 2076-2615 Vol.12 N° 14 2022 págs. 1829ResumenSimple Summary One of the latest goals in regenerative medicine is to use pluripotent stem cells to generate whole organs in vivo through the blastocyst complementation technique. This method consists of the microinjection of pluripotent stem cells into preimplantation embryos that have been genetically modified to ablate the development of a target organ. By taking advantage of the spatiotemporal clues present in the developing embryo, pluripotent stem cells are able to colonize the empty developmental niche and create the missing organ. Combining human pluripotent stem cells with genetically engineered pig embryos, it would be possible to obtain humanized organs that could be used for transplantation, and, therefore, solve the worldwide issue of insufficient availability of transplantable organs. As endothelial cells play a critical role in xenotransplantation rejection in all organs, in this study, we optimized a protocol to generate a vascular-disabled preimplantation pig embryo using the CRISPR/Cas9 system. This protocol could be used to generate avascular embryos for blastocyst complementation experiments and work towards the generation of rejection-free humanized organs in pigs. Each year, tens of thousands of people worldwide die of end-stage organ failure due to the limited availability of organs for use in transplantation. To meet this clinical demand, one of the last frontiers of regenerative medicine is the generation of humanized organs in pigs from pluripotent stem cells (PSCs) via blastocyst complementation. For this, organ-disabled pig models are needed. As endothelial cells (ECs) play a critical role in xenotransplantation rejection in every organ, we aimed to produce hematoendothelial-disabled pig embryos targeting the master transcription factor ETV2 via CRISPR-Cas9-mediated genome modification. In this study, we designed five different guide RNAs (gRNAs) against the DNA-binding domain of the porcine ETV2 gene, which were tested on porcine fibroblasts in vitro. Four out of five guides showed cleavage capacity and, subsequently, these four guides were microinjected individually as ribonucleoprotein complexes (RNPs) into one-cell-stage porcine embryos. Next, we combined the two gRNAs that showed the highest targeting efficiency and microinjected them at higher concentrations. Under these conditions, we significantly improved the rate of biallelic mutation. Hence, here, we describe an efficient one-step method for the generation of hematoendothelial-disabled pig embryos via CRISPR-Cas9 microinjection in zygotes. This model could be used in experimentation related to the in vivo generation of humanized organs.
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Autores: Perelli, S. (Autor de correspondencia); Costa, G. G.; Montiel Terrón, Veronica; et al.Revista: AMERICAN JOURNAL OF SPORTS MEDICINEISSN: 0363-5465 Vol.50 N° 14 2022 págs. 3778 - 3785ResumenBackground: The increase in anterior cruciate ligament (ACL) injuries in pediatric patients and the high failure rate reported in the literature in this population are driving surgeons to search for specific techniques to better restore knee stability. Recent literature has reported that the combination of lateral extra-articular tenodesis (LET) and ACL reconstruction improves outcomes in high-risk patients. However, such advantages in pediatric patients have been infrequently evaluated. Purpose: To assess whether adding LET to ACL reconstruction can significantly improve knee stability, clinical outcomes, and failure rates in pediatric patients. Study Design: Cohort study; Level of evidence, 3. Methods: A multicentric study involving 3 orthopaedic teaching centers was conducted to evaluate pediatric patients aged between 12 and 16 years who had undergone primary ACL reconstruction using a physeal-sparing femoral tunnel drilling technique. A minimum 2-year follow-up evaluation was required. Based on the surgical technique performed, the patients were divided into 2 group. The patients in group 1 underwent an isolated arthroscopic ACL reconstruction, while the patients in group 2 had an arthroscopic ACL reconstruction in combination with a modified Lemaire LET procedure. Group 1 was a historical control cohort of patients, whereas group 2 was prospectively enrolled. All the patients included in the present study were clinically evaluated using the Pediatric International Knee Documentation Committee (Pedi-IKDC) subjective score and the Pediatric Functional Activity Brief Scale (Pedi-FABS) score. Anteroposterior knee stability was measured using the KT-1000 knee ligament arthrometer, and the objective pivot-shift evaluation was documented using a triaxial accelerometer (Kinematic Rapid Assessment [KiRA]). The included patients also underwent a standardized radiological protocol to evaluate leg-length discrepancies, axial deviation, and degenerative signs preoperatively and at last follow-up. Results: This study included 66 pediatric patients with an anatomic hybrid ACL reconstruction using an autologous 4-strand hamstring graft. In group 1, there were 34 patients (mean age, 13.5 +/- 1.2 years), while 32 patients (mean age, 13.8 +/- 1.4 years) were included in group 2. The clinical outcome scores showed no difference between the 2 groups (Pedi-IKDC, P = .072; Pedi-FABS, P = .180). Nevertheless, the patients in group 2 had better anteroposterior stability measured using a KT-1000 arthrometer (1.9 +/- 1.1 mm in group 1 vs 0.8 +/- 0.8 mm in group 2; P = .031), as well as better rotational stability measured using the KiRA (-0.59 +/- 1.05 m/s(2) in group 2 vs 0.98 +/- 1.12 m/s(2) in group 1; P = .012). The patients in group 1 returned to sports at the same competitive level at a rate of 82.4%, while patients included in group 2 returned at the same competitive level in 90.6% of the cases without a significant difference between the 2 groups (P = .059). No leg-length discrepancies were found between the 2 groups at last follow-up (P = .881). Two patients displayed an increased valgus deformity of 3 degrees on the operated limb at last follow-up (1 patient in group 1 and 1 patient in group 2). Group 1 had a significatively higher cumulative failure rate (14.7% vs 6.3%; P = .021). No intra- or postoperative complications was observed between the 2 groups. Conclusion: Performing a modified Lemaire LET along with an ACL reconstruction with hamstring graft in pediatric patients reduced the cumulative failure rate and improved objective stability with no increase in intra- or postoperative complications. No significant difference was found between the 2 groups in terms of patient-reported outcomes or in the return-to-sports activity.
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Autores: Ontoria-Oviedo, I.; Amaro-Prellezo, E.; Castellano, D.; et al.Revista: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCESISSN: 1422-0067 Vol.23 N° 17 2022 págs. 9918ResumenImpaired wound healing in patients with type 2 diabetes (DM2) is characterized by chronic inflammation, which delays wound closure. Specialized pro-resolving lipid mediators (SPMs) are bioactive molecules produced from essential polyunsaturated fatty acids (PUFAs), principally omega-3 docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). SPMs are potent regulators of inflammation and have been used to suppress chronic inflammation in peripheral artery disease, non-alcoholic fatty liver disease, and central nervous system syndromes. LIPINOVA® is a commercially available safe-grade nutritional supplement made from a fractionated marine lipid concentrate derived from anchovy and sardine oil that is rich in SPMs and EPA, as well as DHA precursors. Here, we assessed the effect of LIPINOVA® in wound dressing applications. LIPINOVA® showed biocompatibility with keratinocytes and fibroblasts, reduced the abundance of pro-inflammatory macrophages (M¿1), and promoted in vitro wound closure. Daily application of the marine oil to open wounds made by punch biopsy in db/db mice promoted wound closure by accelerating the resolution of inflammation, inducing neoangiogenesis and M¿1/M¿2 macrophage polarization. In conclusion, LIPINOVA® displays pro-resolutive properties and could be exploited as a therapeutic agent for the treatment of diabetic ulcers.
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Autores: Montero Calle, Maria del Pilar; Flandes Iparraguirre, María; Mountris, K.; et al.Revista: BIOFABRICATIONISSN: 1758-5082 Vol.14 N° 4 2022 págs. 045017ResumenBiofabrication of human tissues has seen a meteoric growth triggered by recent technical advancements such as human induced pluripotent stem cells (hiPSCs) and additive manufacturing. However, generation of cardiac tissue is still hampered by lack of adequate mechanical properties and crucially by the often unpredictable post-fabrication evolution of biological components. In this study we employ melt electrowriting (MEW) and hiPSC-derived cardiac cells to generate fibre-reinforced human cardiac minitissues. These are thoroughly characterized in order to build computational models and simulations able to predict their post-fabrication evolution. Our results show that MEW-based human minitissues display advanced maturation 28 post-generation, with a significant increase in the expression of cardiac genes such as MYL2, GJA5, SCN5A and the MYH7/MYH6 and MYL2/MYL7 ratios. Human iPSC-cardiomyocytes are significantly more aligned within the MEW-based 3D tissues, as compared to conventional 2D controls, and also display greater expression of C x43. These are also correlated with a more mature functionality in the form of faster conduction velocity. We used these data to develop simulations capable of accurately reproducing the experimental performance. In-depth gauging of the structural disposition (cellular alignment) and intercellular connectivity (C x43) allowed us to develop an improved computational model able to predict the relationship between cardiac cell alignment and functional performance. This study lays down the path for advancing in the development of in silico tools to predict cardiac biofabricated tissue evolution after generation, and maps the route towards more accurate and biomimetic tissue manufacture.
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Autores: Pérez Estenaga, Íñigo; Chevalier, M. T.; Pena, E.; et al.Revista: EUROPEAN JOURNAL OF HEART FAILUREISSN: 1388-9842 Vol.24 N° Suppl. 2 2022 págs. 43 - 44
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Autores: Ozkan, H.; Valdés Fernández, José; Willcockson, H. H.; et al.Revista: OSTEOARTHRITIS AND CARTILAGEISSN: 1063-4584 Vol.30 N° Suppl. 1 2022 págs. S293 - S294
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Autores: Mazo Vega, Manuel María; Montero Calle, Maria del Pilar; Flandes Iparraguirre, María; et al.Revista: TISSUE ENGINEERING PART AISSN: 1937-3341 Vol.28 N° Supl. 1 2022 págs. S129
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Autores: Tadevosyan, K.; Iglesias García, Olalla (Autor de correspondencia); Mazo Vega, Manuel María; et al.Revista: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCESISSN: 1422-0067 Vol.22 N° 3 2021 págs. 1479ResumenCardiac tissue engineering is very much in a current focus of regenerative medicine research as it represents a promising strategy for cardiac disease modelling, cardiotoxicity testing and cardiovascular repair. Advances in this field over the last two decades have enabled the generation of human engineered cardiac tissue constructs with progressively increased functional capabilities. However, reproducing tissue-like properties is still a pending issue, as constructs generated to date remain immature relative to native adult heart. Moreover, there is a high degree of heterogeneity in the methodologies used to assess the functionality and cardiac maturation state of engineered cardiac tissue constructs, which further complicates the comparison of constructs generated in different ways. Here, we present an overview of the general approaches developed to generate functional cardiac tissues, discussing the different cell sources, biomaterials, and types of engineering strategies utilized to date. Moreover, we discuss the main functional assays used to evaluate the cardiac maturation state of the constructs, both at the cellular and the tissue levels. We trust that researchers interested in developing engineered cardiac tissue constructs will find the information reviewed here useful. Furthermore, we believe that providing a unified framework for comparison will further the development of human engineered cardiac tissue constructs displaying the specific properties best suited for each particular application.
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Autores: Moya-Garzón, M. D.; Gómez-Vidal, J. A.; Alejo-Armijo, A.; et al.Revista: JOURNAL OF PERSONALIZED MEDICINEISSN: 2075-4426 Vol.11 N° 2 2021 págs. 74ResumenPrimary hyperoxalurias (PHs) are a group of inherited alterations of the hepatic glyoxylate metabolism. PHs classification based on gene mutations parallel a variety of enzymatic defects, and all involve the harmful accumulation of calcium oxalate crystals that produce systemic damage. These geographically widespread rare diseases have a deep impact in the life quality of the patients. Until recently, treatments were limited to palliative measures and kidney/liver transplants in the most severe forms. Efforts made to develop pharmacological treatments succeeded with the biotechnological agent lumasiran, a siRNA product against glycolate oxidase, which has become the first effective therapy to treat PH1. However, small molecule drugs have classically been preferred since they benefit from experience and have better pharmacological properties. The development of small molecule inhibitors designed against key enzymes of glyoxylate metabolism is on the focus of research. Enzyme inhibitors are successful and widely used in several diseases and their pharmacokinetic advantages are well known. In PHs, effective enzymatic targets have been determined and characterized for drug design and interesting inhibitory activities have been achieved both in vitro and in vivo. This review describes the most recent advances towards the development of small molecule enzyme inhibitors in the treatment of PHs, introducing the multi-target approach as a more effective and safe therapeutic option.
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Autores: Lamo de Espinosa Vázquez de Sola, José María; Prosper Cardoso, Felipe; Blanco, J. F.; et al.Revista: JOURNAL OF TRANSLATIONAL MEDICINEISSN: 1479-5876 Vol.19 N° 1 2021 págs. 506ResumenKnee osteoarthritis is the most prevalent joint disease and a frequent cause of pain, functional loss and disability. Conventional treatments have demonstrated only modest clinical benefits whereas cell-based therapies have shown encouraging results, but important details, such as dose needed, long-term evolution or number of applications required are scarcely known. Here we have reanalyzed results from two recent pilot trials with autologous bone marrow-derived mesenchymal stromal cells using the Huskisson plot to enhance quantification of efficacy and comparability. We find that cell doses of 10, 40 and 100 million autologous cells per knee provided quite similar healing results and that much of the effect attained 1 year after cell application remained after 2 and 4 years. These results are encouraging because they indicate that, apart from safety and simplicity: (i) the beneficial effect is both significant and sizeable, (ii) it can be achieved with a single injection of cells, and (iii) the effect is perdurable for years.
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Autores: Soria-Juan, B.; García-Arranz, M.; Jiménez, L. L.; et al.Revista: TRIALSISSN: 1745-6215 Vol.22 N° 1 2021 págs. 595ResumenBackground: Chronic lower limb ischemia develops earlier and more frequently in patients with type 2 diabetes mellitus. Diabetes remains the main cause of lower-extremity non-traumatic amputations. Current medical treatment, based on antiplatelet therapy and statins, has demonstrated deficient improvement of the disease. In recent years, research has shown that it is possible to improve tissue perfusion through therapeutic angiogenesis. Both in animal models and humans, it has been shown that cell therapy can induce therapeutic angiogenesis, making mesenchymal stromal cell-based therapy one of the most promising therapeutic alternatives. The aim of this study is to evaluate the feasibility, safety, and efficacy of cell therapy based on mesenchymal stromal cells derived from adipose tissue intramuscular administration to patients with type 2 diabetes mellitus with critical limb ischemia and without possibility of revascularization. Methods: A multicenter, randomized double-blind, placebo-controlled trial has been designed. Ninety eligible patients will be randomly assigned at a ratio 1:1:1 to one of the following: control group (n = 30), low-cell dose treatment group (n = 30), and high-cell dose treatment group (n = 30). Treatment will be administered in a single-dose way and patients will be followed for 12 months. Primary outcome (safety) will be evaluated by measuring the rate of adverse events within the study period. Secondary outcomes (efficacy) will be measured by assessing clinical, analytical, and imaging-test parameters. Tertiary outcome (quality of life) will be evaluated with SF-12 and VascuQol-6 scales. Discussion: Chronic lower limb ischemia has limited therapeutic options and constitutes a public health problem in both developed and underdeveloped countries. Given that the current treatment is not established in daily clinical practice, it is essential to provide evidence-based data that allow taking a step forward in its clinical development. Also, the multidisciplinary coordination exercise needed to develop this clinical trial protocol will undoubtfully be useful to conduct academic clinical trials in the field of cell therapy in the near future.
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Autores: Montiel Terrón, Veronica (Autor de correspondencia); Vitoria Sola, María; Lamo de Espinosa Vázquez de Sola, José María; et al.Revista: ARCHIVES OF ORTHOPAEDIC AND TRAUMA SURGERYISSN: 1434-3916 Vol.141 N° 2 2021 págs. 313 - 319ResumenIntroduction The knee in Parkinson's disease (PD) patients is a problematic joint due to pain, stiffness and gait instability. The aim of this study is to evaluate the functional outcome and degree of pain relief achieved after total knee arthroplasty (TKA) in PD patients. Materials and methods This is a retrospective review of 26 PD patients (32 knees) with osteoarthritis who underwent a TKA between 1994 and 2013. Comorbidities, anesthetic procedures and complications were recorded. Patient functional status was assessed with the Knee Society Function Score (KFS) and the Knee Society Score (KSS). PD stage was classified with the Hoehn and Yahr Scale. Results The mean follow-up was 3.5 years (range 2-9). The mean age was 71 years (range 61-83) with a mean time since PD diagnosis of 11.8 years (range 4-24). PD severity on the Hoehn and Yahr Scale was 1.5 points before surgery and 2 points postoperatively. Pain on the visual analogic scale improved from 8 points preoperatively to 5 points at 1-year follow-up; function improved from 32 (range 20-45) to 71 (range 50-81) and from 34 (range 28-52) to 59 (range 25-76) on the KSS and KFS, respectively. The mean postoperative hospital stay was 9.8 days (range 5-21). Confusion and flexion contracture were the most frequent perioperative complications. Conclusion TKA successfully provided pain relief in PD patients. However, the functional outcome is related to disease progression and, therefore, variable. Perioperative complications are difficult to avoid and manage.
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Autores: Perez-Prieto, D. (Autor de correspondencia); Perelli, S.; Corcoll, F. ; et al.Título: The vancomycin soaking technique: no differences in autograft re-rupture rate. A comparative studyRevista: INTERNATIONAL ORTHOPAEDICSISSN: 0341-2695 Vol.45 N° 6 2021 págs. 1407 - 1411ResumenPurpose The main aim of this study was to evaluate the re-rupture risk after an anterior cruciate ligament reconstruction (ACL-R) using the vancomycin soaking technique and to compare it with the re-rupture risk in patients on whom this technique was not utilized. The secondary purpose was to compare the functional outcomes of those two subsets of patients operated on for ACL-R. The hypotheses are that the vancomycin soaking technique does not affect the re-rupture risk or the functional outcomes. Material and methods A retrospective historical cohort study was conducted. Two groups were compared in terms of the re-rupture rate (traumatic or atraumatic) and functional outcomes (International Knee Documentation Committee (IKDC), Tegner, and Lysholm). Group 1 consisted of patients that received pre-operative IV antibiotics. In group 2, the patients received pre-operative IV antibiotics along with a graft that had been presoaked in a vancomycin solution. A minimum follow-up of five years was required. Results There were 17 patients that suffered a re-rupture in group 1 (4.7%) and 15 in group 2 (3.9%) (n.s.). IKDC was 82.0 in group 1 and 83.9 in group 2 (p = 0.049); Tegner scored 4 in both groups (n.s.) and Lysholm was 90.3 in group 1 and 92.0 in group 2 (p = 0.015). Conclusion The vancomycin soaking technique for ACL autografts is a safe procedure for the daily clinical practice, in terms of re-ruptures. Moreover, it does not impair functional outcomes after an ACL-R.
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Autores: López Díaz de Cerio, Ascensión; Pérez Estenaga, Íñigo; Inoges Sancho, Susana Inmaculada; et al.Revista: PHARMACEUTICSISSN: 1999-4923 Vol.13 N° 8 2021 págs. 1269ResumenThe use of allogeneic adipose-derived mesenchymal stromal cells (alloADSCs) represents an attractive approach for treating myocardial infarction (MI). Furthermore, adding a natural support improves alloADSCs engraftment and survival in heart tissues, leading to a greater therapeutic effect. We aimed to examine the safety and immunological reaction induced by epicardial implantation of a clinical-grade collagen scaffold (CS) seeded with alloADSCs for its future application in humans. Thus, cellularized scaffolds were myocardially or subcutaneously implanted in immunosuppressed rodent models. The toxicological parameters were not significantly altered, and tumor formation was not found over the short or long term. Furthermore, biodistribution analyses in the infarcted immunocompetent rats displayed cell engraftment in the myocardium but no migration to other organs. The immunogenicity of alloADSC-CS was also evaluated in a preclinical porcine model of chronic MI; no significant humoral or cellular alloreactive responses were found. Moreover, CS cellularized with human ADSCs cocultured with human allogeneic immune cells produced no alloreactive response. Interestingly, alloADSC-CS significantly inhibited lymphocyte responses, confirming its immunomodulatory action. Thus, alloADSC-CS is likely safe and does not elicit any alloreactive immunological response in the host. Moreover, it exerts an immunomodulatory action, which supports its translation to a clinical setting.
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Autores: Abizanda Sarasa, Gloria María; López Muneta, Leyre; Linares Acosta, Javier; et al.Revista: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCESISSN: 1422-0067 Vol.22 N° 17 2021 págs. 9126ResumenThe success of cell therapy for the treatment of myocardial infarction depends on finding novel approaches that can substantially implement the engraftment of the transplanted cells. In order to enhance cell engraftment, most studies have focused on the pretreatment of transplantable cells. Here we have considered an alternative approach that involves the preconditioning of infarcted heart tissue to reduce endogenous cell activity and thus provide an advantage to our exogenous cells. This treatment is routinely used in other tissues such as bone marrow and skeletal muscle to improve cell engraftment, but it has never been taken in cardiac tissue. To avoid long-term cardiotoxicity induced by full heart irradiation we developed a rat model of a catheter-based heart irradiation system to locally impact a delimited region of the infarcted cardiac tissue. As proof of concept, we transferred ZsGreen(+) iPSCs in the infarcted heart, due to their ease of use and detection. We found a very significant increase in cell engraftment in preirradiated rats. In this study, we demonstrate for the first time that preconditioning the infarcted cardiac tissue with local irradiation can substantially enhance cell engraftment.
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Autores: Vera Álvarez, Laura; García Olloqui, Paula; Petri González, Eva; et al.Revista: AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGYISSN: 1044-1549 Vol.64 N° 4 2021 págs. 465 - 476ResumenFibroblast activation includes differentiation to myofibroblasts and is a key feature of organ fibrosis. The Notch pathway has been involved in myofibroblast differentiation in several tissues, including the lung. Here, we identify a subset of collagen-expressing cells in the lung that exhibit Notch3 activity at homeostasis. After injury, this activation increases, being found in alpha SMA-expressing myofibroblasts in the mouse and human fibrotic lung. Although previous studies suggest a contribution of Notch3 in stromal activation, in vivo evidence of the role of Notch3 in lung fibrosis remains unknown. In this study, we examine the effects of Notch3 deletion in pulmonary fibrosis and demonstrate that Notch3-deficient lungs are protected from lung injury with significantly reduced collagen deposition after bleomycin administration. The induction of profibrotic genes is reduced in bleomycin-treated Notch3-knockout lungs that consistently present fewer alpha SMA-positive myofibroblasts. As a result, the volume of healthy lung tissue is higher and lung function is improved in the absence of Notch3. Using in vitro cultures of lung primary fibroblasts, we confirmed that Notch3 participates in their survival and differentiation. Thus, Notch3 deficiency mitigates the development of lung fibrosis because of its role in mediating fibroblast activation. Our findings reveal a previously unidentified mechanism underlying lung fibrogenesis and provide a potential novel therapeutic approach to target pulmonary fibrosis.
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Autores: Baraibar Churio, Arantxa; Bobadilla Muñoz, Miriam; Machado, F. J. D.; et al.Revista: LIFEISSN: 2075-1729 Vol.11 N° 12 2021 págs. 1398ResumenMatrix metalloproteinases (MMPs) have been implicated in the progression of muscular dystrophy, and recent studies have reported the role of MMP-10 in skeletal muscle pathology of young dystrophic mice. Nevertheless, its involvement in dystrophin-deficient hearts remains unexplored. Here, we aimed to investigate the involvement of MMP-10 in the progression of severe muscular dystrophy and to characterize MMP-10 loss in skeletal and cardiac muscles of aged dystrophic mice. We examined the histopathological effect of MMP-10 ablation in aged mdx mice, both in the hind limb muscles and heart tissues. We found that MMP-10 loss compromises survival rates of aged mdx mice, with skeletal and cardiac muscles developing a chronic inflammatory response. Our findings indicate that MMP-10 is implicated in severe muscular dystrophy progression, thus identifying a new area of research that could lead to future therapies for dystrophic muscles.
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Autores: Yañez Arauz, J. M.; Yañez Arauz, J. M.; Montiel Terrón, Veronica; et al.Revista: REVISTA DE LA ASOCIACION ARGENTINA DE ORTOPEDIA Y TRAUMATOLOGIAISSN: 1515-1786 Vol.86 N° 2 2021 págs. 139 - 150ResumenIntroducción: Las técnicas para corregir las deformidades del hallux incluyen osteotomías metatarsianas y falángicas. Las osteotomías sobre la falange proximal corrigen el DASA y el ángulo interfalángico. Sin embargo, no se han publicado las indicaciones para la osteotomía de la falange distal. El objetivo de este artículo es comunicar la técnica y las indicaciones de la osteotomía percutánea de la falange distal del hallux, y evaluar los resultados de una serie de casos. Materiales y Métodos: Se analizaron 14 pies en los que se realizó una osteotomía de la falange distal del hallux para corregir una deformidad. Se midieron el DASA, la oblicuidad interfalángica y el ángulo falange distal-interfalángico en las radiografías. La técnica quirúrgica fue percutánea con control fluoroscópico. Los resultados se evaluaron mediante las escalas analógica visual de dolor y AOFAS. Seguimiento medio: 52 meses. Resultados: 13 pies de mujeres y un pie de hombre. Edad promedio: 58 años. Los resultados clínico y estético fueron excelentes, con alivio del dolor. Mejoría de la escala AOFAS: promedio 37 puntos. Análisis comparativo de ángulos preoperatorios y posoperatorios: DASA (p = 0,01), excepto cuando se aisló de la muestra a los pacientes con osteotomía tipo Akin (p = 0,33); ángulos F2-IF y F2-MTF (p <0,00001). Se registraron las complicaciones. Conclusiones: En la deformidad en valgo de la falange distal del hallux sintomática, se debe considerar una osteotomía correctora sola o asociada a osteotomía de la falange proximal. La osteotomía percutánea de la falange distal es un método eficaz, seguro y rápido. Nivel de Evidencia: IV
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Autores: Torres, A. G.; Rodríguez-Escribà, M.; Marcet-Houben, M.; et al.Revista: NUCLEIC ACIDS RESEARCHISSN: 0305-1048 Vol.49 N° 12 2021 págs. 7011 - 7034ResumenThe modification of adenosine to inosine at the wobble position (134) of tRNA anticodons is an abundant and essential feature of eukaryotic tRNAs. The expansion of inosine-containing tRNAs in eukaryotes followed the transformation of the homodimeric bacterial enzyme TadA, which generates 134 in tRNA(Arg) and tRNA(Leu), into the heterodimeric eukaryotic enzyme ADAT, which modifies up to eight different tRNAs. The emergence of ADAT and its larger set of substrates, strongly influenced the tRNA composition and codon usage of eukaryotic genomes. However, the selective advantages that drove the expansion of 134-tRNAs remain unknown. Here we investigate the functional relevance of 134-tRNAs in human cells and show that a full complement of these tRNAs is necessary for the translation of low-complexity protein domains enriched in amino acids cognate for 134-tRNAs. The coding sequences for these domains require codons translated by 134-tRNAs, in detriment of synonymous codons that use other tRNAs. 134-tRNA-dependent low-complexity proteins are enriched in functional categories related to cell adhesion, and depletion in 134-tRNAs leads to cellular phenotypes consistent with these roles. We show that the distribution of these low-complexity proteins mirrors the distribution of 134-tRNAs in the phylogenetic tree.
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Autores: Valdés Fernández, José (Autor de correspondencia); López-Martínez, T.; Ripalda Cemborain, Purificación; et al.Título: Molecular and Cellular Mechanisms of Delayed Fracture Healing in Mmp10 (Stromelysin 2) Knockout MiceRevista: JOURNAL OF BONE AND MINERAL RESEARCHISSN: 0884-0431 Vol.36 N° 11 2021 págs. 2203 - 2213ResumenThe remodeling of the extracellular matrix is a central function in endochondral ossification and bone homeostasis. During secondary fracture healing, vascular invasion and bone growth requires the removal of the cartilage intermediate and the coordinate action of the collagenase matrix metalloproteinase (MMP)-13, produced by hypertrophic chondrocytes, and the gelatinase MMP-9, produced by cells of hematopoietic lineage. Interfering with these MMP activities results in impaired fracture healing characterized by cartilage accumulation and delayed vascularization. MMP-10, Stromelysin 2, a matrix metalloproteinase with high homology to MMP-3 (Stromelysin 1), presents a wide range of putative substrates identified in vitro, but its targets and functions in vivo and especially during fracture healing and bone homeostasis are not well defined. Here, we investigated the role of MMP-10 through bone regeneration in C57BL/6 mice. During secondary fracture healing, MMP-10 is expressed by hematopoietic cells and its maximum expression peak is associated with cartilage resorption at 14 days post fracture (dpf). In accordance with this expression pattern, when Mmp10 is globally silenced, we observed an impaired fracture-healing phenotype at 14 dpf, characterized by delayed cartilage resorption and TRAP-positive cell accumulation. This phenotype can be rescued by a non-competitive transplant of wild-type bone marrow, indicating that MMP-10 functions are required only in cells of hematopoietic linage. In addition, we found that this phenotype is a consequence of reduced gelatinase activity and the lack of proMMP-9 processing in macrophages. Our data provide evidence of the in vivo function of MMP-10 during endochondral ossification and defines the macrophages as the lead cell population in cartilage removal and vascular invasion. (c) 2021 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).
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Autores: Salterain González, Nahikari; Ibero Valencia, Javier; Riesgo García, Álvaro; et al.Revista: JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGYISSN: 0735-1097 Vol.77 N° 18 Supl. 1 2021 págs. 854 - 854
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Autores: Wu, M.; Claus, P.; De Buck, S.; et al.Revista: EUROPEAN HEART JOURNALISSN: 0195-668X Vol.42 N° Supl. 1 2021 págs. 912
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Autores: Sáenz Idoate, Víctor; Salterain González, Nahikari; Torres Santamaría, María José; et al.Título: Utility of amily score for transthyretin amyloidosis patients in daily practice: easy and simpleRevista: EUROPEAN JOURNAL OF HEART FAILUREISSN: 1388-9842 Vol.23 N° Supl. 2 2021 págs. 29 - 30
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Autores: Reverter, E.; Juanola, A.; Prado, V.; et al.Revista: JOURNAL OF HEPATOLOGY (ONLINE)ISSN: 0168-8278 Vol.75 N° Supl. 2 2021 págs. S329 - S330
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Autores: Tamayo, L.; Tamayo Uria, Ibon; Vales Aranguren, África; et al.Revista: JOURNAL OF HEPATOLOGY (ONLINE)ISSN: 0168-8278 Vol.75 N° Supl. 2 2021 págs. S694 - S694
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Autores: Calviño Sampedro, Cristina; Ceballos, C.; Inoges Sancho, Susana Inmaculada; et al.Revista: HUMAN GENE THERAPYISSN: 1043-0342 Vol.32 N° 19-20 2021 págs. A36 - A37
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Autores: Díaz Mazquiaran, Aintzane; de la Fuente Cedeño, J.; SERRANO SANZ, Guillermo; et al.Revista: HAEMATOLOGICAISSN: 0390-6078 Vol.106 N° 10 s2 2021 págs. 100 - 101
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Autores: Molinos-Vicente, A.; García-Torralba, A.; Nieto-Romero, V.; et al.Revista: MOLECULAR THERAPYISSN: 1525-0016 Vol.29 N° 4 2021 págs. 246 - 246
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Autores: Montero Calle, Maria del Pilar; Flandes Iparraguirre, María; Musquiz, S.; et al.Revista: ECLINICALMEDICINEISSN: 2589-5370 Vol.8 2020 págs. 955ResumenCardiovascular disease is the number one killer worldwide, with myocardial infarction (MI) responsible for approximately 1 in 6 deaths. The lack of endogenous regenerative capacity, added to the deleterious remodelling programme set into motion by myocardial necrosis, turns MI into a progressively debilitating disease, which current pharmacological therapy cannot halt. The advent of Regenerative Therapies over 2 decades ago kick-started a whole new scientific field whose aim was to prevent or even reverse the pathological processes of MI. As a highly dynamic organ, the heart displays a tight association between 3D structure and function, with the non-cellular components, mainly the cardiac extracellular matrix (ECM), playing both fundamental active and passive roles. Tissue engineering aims to reproduce this tissue architecture and function in order to fabricate replicas able to mimic or even substitute damaged organs. Recent advances in cell reprogramming and refinement of methods for additive manufacturing have played a critical role in the development of clinically relevant engineered cardiovascular tissues. This review focuses on the generation of human cardiac tissues for therapy, paying special attention to human pluripotent stem cells and their derivatives. We provide a perspective on progress in regenerative medicine from the early stages of cell therapy to the present day, as well as an overview of cellular processes, materials and fabrication strategies currently under investigation. Finally, we summarise current clinical applications and reflect on the most urgent needs and gaps to be filled for efficient translation to the clinical arena.
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Autores: López Muneta, Leyre; Miranda-Arrubla, J.; Carvajal Vergara, Xonia (Autor de correspondencia)Revista: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCESISSN: 1422-0067 Vol.21 N° 21 2020 págs. 7950ResumenDirect cardiac reprogramming has emerged as a novel therapeutic approach to treat and regenerate injured hearts through the direct conversion of fibroblasts into cardiac cells. Most studies have focused on the reprogramming of fibroblasts into induced cardiomyocytes (iCMs). The first study in which this technology was described, showed that at least a combination of three transcription factors, GATA4, MEF2C and TBX5 (GMT cocktail), was required for the reprogramming into iCMs in vitro using mouse cells. However, this was later demonstrated to be insufficient for the reprogramming of human cells and additional factors were required. Thereafter, most studies have focused on implementing reprogramming efficiency and obtaining fully reprogrammed and functional iCMs, by the incorporation of other transcription factors, microRNAs or small molecules to the original GMT cocktail. In this respect, great advances have been made in recent years. However, there is still no consensus on which of these GMT-based varieties is best, and robust and highly reproducible protocols are still urgently required, especially in the case of human cells. On the other hand, apart from CMs, other cells such as endothelial and smooth muscle cells to form new blood vessels will be fundamental for the correct reconstruction of damaged cardiac tissue. With this aim, several studies have centered on the direct reprogramming of fibroblasts into induced cardiac progenitor cells (iCPCs) able to give rise to all myocardial cell lineages. Especially interesting are reports in which multipotent and highly expandable mouse iCPCs have been obtained, suggesting that clinically relevant amounts of these cells could be created. However, as of yet, this has not been achieved with human iCPCs, and exactly what stage of maturity is appropriate for a cell therapy product remains an open question. Nonetheless, the major concern in regenerative medicine is the poor retention, survival, and engraftment of transplanted cells in the cardiac tissue. To circumvent this issue, several cell pre-conditioning approaches are currently being explored. As an alternative to cell injection, in vivo reprogramming may face fewer barriers for its translation to the clinic. This approach has achieved better results in terms of efficiency and iCMs maturity in mouse models, indicating that the heart environment can favor this process. In this context, in recent years some studies have focused on the development of safer delivery systems such as Sendai virus, Adenovirus, chemical cocktails or nanoparticles. This article provides an in-depth review of the in vitro and in vivo cardiac reprograming technology used in mouse and human cells to obtain iCMs and iCPCs, and discusses what challenges still lie ahead and what hurdles are to be overcome before results from this field can be transferred to the clinical settings.
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Autores: Lamo de Espinosa Vázquez de Sola, José María (Autor de correspondencia); Blanco, J. F. ; Sanchez, M.; et al.Revista: JOURNAL OF TRANSLATIONAL MEDICINEISSN: 1479-5876 Vol.18 N° 1 2020 págs. 356ResumenBackground Mesenchymal stromal cells are a safe and promising option to treat knee osteoarthritis as previously demonstrated in different clinical trials. However, their efficacy, optimal dose and addition of adjuvants must be determined. Here, we evaluated the clinical effects of a dose of 100 x 10(6)bone marrow mesenchymal stromal cells (BM-MSCs) in combination with Platelet Rich Plasma (PRGF (R)) as adjuvant in a randomized clinical trial. Methods A phase II, multicenter, randomized clinical trial with active control was conducted. Sixty patients diagnosed with knee OA were randomly assigned to 3 weekly doses of PRGF (R) or intraarticular administration of 100 x 10(6)cultured autologous BM-MSCs plus PRGF (R). Patients were followed up for 12 months, and pain and function were assessed using VAS and WOMAC and by measuring the knee range of motion range. X-ray and magnetic resonance imaging analyses were performed to analyze joint damage. Results No adverse effects were reported after BM-MSC administration or during follow-up. According to VAS, the mean value (SD) for PRGF (R) and BM-MSC with PRGF (R) went from 5 (1.8) to 4.5 (2.2) (p = 0.389) and from 5.3 (1.9) to 3.5 (2.5) (p = 0.01), respectively at 12 months. In WOMAC, the mean (SD) baseline and 12-month overall WOMAC scores in patients treated with PRGF (R) was 31.9 (16.2) and 22.3 (15.8) respectively (p = 0.002) while that for patients treated with BM-MSC plus PRGF (R) was 33.4 (18.7) and 23.0 (16.6) (p = 0.053). Although statistical significances between groups have been not detected, only patients being treated with BM-MSC plus PRGF (R) could be considered as a OA treatment responders following OARSI criteria. X-ray and MRI (WORMS protocol) revealed no changes in knee joint space width or joint damage. Conclusions Treatment with BM-MSC associated with PRGF (R) was shown to be a viable therapeutic option for osteoarthritis of the knee, with clinical improvement at the end of follow-up. Further phase III clinical trials would be necessary to confirm the efficacy. Trial registrationClinical Trials.gov identifier NCT02365142. No EudraCT: 2011-006036-23
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Autores: Pons de Villanueva, Juan; Rodríguez Díez, María CristinaTítulo: Me duele el codoLibro: Manual de casos con pacientes estandarizados para el ECOEISSN: 978-84-9110-942-6 2022 págs. 34 - 36
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Autores: Pelacho Samper, Beatriz; Pérez Ruiz, Ana Isabel; Prosper Cardoso, FelipeLibro: Platelet rich plasma in orthopaedics and sports medicineISSN: 978-3-319-63729-7 2018 págs. 83 - 97
Proyectos desde 2018
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Título: Desarrollo de Medicamentos Innovadores basados en CAR-T: Datos, Inteligencia Artificial, secuenciación MAsiva y Nano-Tecnología (DIAMANTE). Proyecto financiado en el marco de la convocatoria 2023 de proyectos Estratégicos de Gobierno de NavarraCódigo de expediente: 0011-1411-2023-000105Investigador principal: FELIPE LUIS PROSPER CARDOSO.Financiador: GOBIERNO DE NAVARRAConvocatoria: 2023 GN PROYECTOS ESTRATEGICOS DE I+D 2023-2026Fecha de inicio: 01-07-2023Fecha fin: 31-12-2025Importe concedido: 362.076,16€Otros fondos: -
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Título: Estrategias de tratamiento temprano de la osteomielitis en la prevención de la pseudoartrosis de fracturaCódigo de expediente: GN2022/06Investigador principal: FROILAN GRANERO MOLTO.Financiador: GOBIERNO DE NAVARRA. DEPARTAMENTO DE SALUDConvocatoria: 2022 GN Proyectos de Investigación en saludFecha de inicio: 22-12-2022Fecha fin: 21-12-2024Importe concedido: 48.875,00€Otros fondos: -
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Título: DeSarrollO de terapias CAR-T innovadoras para el trAtamiento de Tumores Hematológicos y Sólidos (SOCRATHeS)Código de expediente: 0011-1411-2022-000053Investigador principal: FELIPE LUIS PROSPER CARDOSO, FELIPE LUIS PROSPER CARDOSO.Financiador: GOBIERNO DE NAVARRAConvocatoria: 2022 GN PROYECTOS ESTRATEGICOS DE I+D 2022-2025Fecha de inicio: 01-05-2022Fecha fin: 30-12-2024Importe concedido: 371.489,00€Otros fondos: -
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Título: Terapias avanzadasCódigo de expediente: RD21/0017/0009Investigador principal: FELIPE LUIS PROSPER CARDOSO.Financiador: INSTITUTO DE SALUD CARLOS IIIConvocatoria: 2021 AES Redes de Investigación cooperativa orientadas a resultados (RICORS)Fecha de inicio: 01-01-2022Fecha fin: 31-12-2024Importe concedido: 94.947,60€Otros fondos: Fondos FEDER
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Título: New targets and designs to improve CAR-T cell based immunotherapy against pancreatic cancer (CarPanTu)Código de expediente: PLEC2021-008094Investigador principal: FELIPE LUIS PROSPER CARDOSO.Financiador: AGENCIA ESTATAL DE INVESTIGACIONConvocatoria: 2021 AEI Proyectos de I+D+i en líneas estratégicasFecha de inicio: 01-11-2021Fecha fin: 31-10-2024Importe concedido: 100.042,00€Otros fondos: Fondos MRR
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Título: Estudio genómico para la personalización del diagnóstico y el tratamiento de los pacientes con insuficiencia Cardíaca crónica y enfermedad renal crónica (Medicina cardIoreNal pERsonalizada en NaVArra)-II (MINERVA-II)Código de expediente: 0011-1411-2021-000094Investigador principal: JUAN JOSE GAVIRA GOMEZ.Financiador: GOBIERNO DE NAVARRAConvocatoria: 2021 GN PROYECTOS ESTRATEGICOS DE I+D 2021-2024Fecha de inicio: 01-05-2021Fecha fin: 31-12-2023Importe concedido: 100.748,76€Otros fondos: -
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Título: Aplicaciones del estudio multi-ómico de la microbiota al desarrollo de soluciones biotecnológicas innovadoras en el área de la salud (microBiomics)Código de expediente: 0011-1411-2021-000106Investigador principal: MARIA TERESA HERRAIZ BAYOD, MARIA TERESA HERRAIZ BAYOD.Financiador: GOBIERNO DE NAVARRAConvocatoria: 2021 GN PROYECTOS ESTRATEGICOS DE I+D 2021-2024Fecha de inicio: 15-04-2021Fecha fin: 31-12-2023Importe concedido: 366.577,17€Otros fondos: -
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Título: Papel de los mecanimso de regulación trascripcional en la patogenia y el tratamiento de los SMDCódigo de expediente: PI20/01308Investigador principal: FELIPE LUIS PROSPER CARDOSO.Financiador: INSTITUTO DE SALUD CARLOS IIIConvocatoria: 2020 AES Proyectos de investigaciónFecha de inicio: 01-01-2021Fecha fin: 31-12-2023Importe concedido: 275.880,00€Otros fondos: Fondos FEDER
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Título: Periostio mimético: mecanismos de reparación ósea y potencial terapéuticoCódigo de expediente: PI20/00076Investigador principal: FROILAN GRANERO MOLTO.Financiador: INSTITUTO DE SALUD CARLOS IIIConvocatoria: 2020 AES Proyectos de investigaciónFecha de inicio: 01-01-2021Fecha fin: 31-12-2023Importe concedido: 123.420,00€Otros fondos: Fondos FEDER
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Título: Nuevos biomarcadores inmunes para la identificación de grupos de riesgo de sufrir infección grave por COVID¿19 mediante citometría de flujoCódigo de expediente: 0011-3638-2020-000004Investigador principal: JOSE RAMON YUSTE ARA.Financiador: GOBIERNO DE NAVARRA. DEPARTAMENTO DE SALUDConvocatoria: 2020 GN Proyectos de Investigación en saludFecha de inicio: 21-12-2020Fecha fin: 20-12-2021Importe concedido: 34.500,00€Otros fondos: Fondos FEDER
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Título: FPU 2019 PAULA RODRIGUEZ MÁRQUEZ JRRM-JJLCódigo de expediente: FPU19/06160Investigador principal: PAULA RODRIGUEZ MARQUEZ.Financiador: MINISTERIO DE CIENCIA E INNOVACIÓNConvocatoria: FIMA 2019 - MINECO BECAS FPU FIMA 2019 - MINECO BECAS FPUFecha de inicio: 15-10-2020Fecha fin: 02-12-2022Importe concedido: 60.268,98€Otros fondos: Fondos FEDER
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Título: Alianza en Genómica Avanzada para el desarrollo de Terapias Personalizadas en NavarraCódigo de expediente: 0011-1411-2020-000010Investigador principal: FELIPE LUIS PROSPER CARDOSO.Financiador: GOBIERNO DE NAVARRAConvocatoria: FIMA 2020 GN PROYECTOS ESTRATEGICOS DE I+D 2020-2022Fecha de inicio: 17-06-2020Fecha fin: 30-11-2022Importe concedido: 725.480,08€Otros fondos: -
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Título: Transcriptional and gene regulatory networks in acute myeloid leukemia secondary to myelodysplastic syndromes: identification of novel therapeutic targetsCódigo de expediente: 0011-0537-2019-000001Investigador principal: NEREA BERASTEGUI ZUFIAURRE.Financiador: GOBIERNO DE NAVARRA / DPTO. EDUCACIÓN CULTURA Y TURISMOConvocatoria: FIMA GNE 2019 BECAS PREDOCTORALESFecha de inicio: 01-06-2020Fecha fin: 01-10-2023Importe concedido: 68.715,96€Otros fondos: -
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Título: Incapacitación de las células endógenas del tejido cardiaco dañado para aumentar el injerto de los progenitores cardiovasculares trasplantadosCódigo de expediente: PID2019-107150RB-I00Investigador principal: XONIA CARVAJAL VERGARA.Financiador: MINISTERIO DE CIENCIA E INNOVACIÓNConvocatoria: FIMA 2019 MCIU - AEI PROYECTOS DE I+D RETOS INVESTIGACIONFecha de inicio: 01-06-2020Fecha fin: 22-11-2021Importe concedido: 121.000,00€Otros fondos: Fondos FEDER
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Título: Quimerismo inter-especie y edición génica en embriones de cerdo: QuimPigCódigo de expediente: 0011-1365-2020-000293Investigador principal: XABIER ARANGUREN LOPEZ.Financiador: GOBIERNO DE NAVARRAConvocatoria: FIMA 2020 GN I+D EMPRESAS (Transferencia del conocimiento 2020) QuimPigFecha de inicio: 01-04-2020Fecha fin: 30-07-2022Importe concedido: 172.973,35€Otros fondos: Fondos FEDER
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Título: IDENTIFICACIÓN Y DESARROLLO DE TCR TRANSGÉNICOS PARA TERAPIA CELULAR ADOPTIVA DE TUMORES SÓLIDOSCódigo de expediente: 0011-1383-2020-000010 PC197Investigador principal: SUSANA INMACULADA INOGES SANCHO.Financiador: GOBIERNO DE NAVARRAConvocatoria: 2020 GN Proyectos ColaborativosFecha de inicio: 01-12-2019Fecha fin: 30-11-2022Importe concedido: 137.325,00€Otros fondos: -
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Título: IJCI-2017-33070 GIULIA COPPIELLO FPCódigo de expediente: IJCI-2017-33070Investigador principal: GIULIA COPPIELLO .Financiador: MINISTERIO DE CIENCIA E INNOVACIÓNConvocatoria: 2017 - JUAN DE LA CIERVA INCORPORACION 2017 - JUAN DE LA CIERVA INCORPORACIONFecha de inicio: 01-04-2019Fecha fin: 31-08-2021Importe concedido: 76.156,16€Otros fondos: Fondos FEDER
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Título: Ecosystem of hematopoietic stem cell: Manipulation of the niche for therapeutic useCódigo de expediente: 0011-0537-2018-000008Investigador principal: ANA CRISTINA VIÑADO SOLANAS.Financiador: GOBIERNO DE NAVARRA / DPTO. EDUCACIÓN CULTURA Y TURISMOConvocatoria: GNE 2018 BECAS PREDOCTORALESFecha de inicio: 01-04-2019Fecha fin: 31-03-2022Importe concedido: 68.718,00€Otros fondos: -
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Título: Caracterización bioinformática, del perfil transcriptómico y epigenético de células madre hematopoyéticas (CD34+). Integración de ambas tecnologías genómicas para identificar "gene regulatory networks"Código de expediente:Investigador principal: MARINA AINCIBURU FERNANDEZ.Financiador: GOBIERNO DE NAVARRA / DPTO. EDUCACIÓN CULTURA Y TURISMOConvocatoria: GNE 2018 BECAS PREDOCTORALESFecha de inicio: 01-04-2019Fecha fin: 08-09-2019Importe concedido: 68.718,00€Otros fondos: Fondos FEDER
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Título: Desarrollo de estructuras 3D para igeniería de tejidosCódigo de expediente: 0011-1383-2019-000005 PC074Investigador principal: FROILAN GRANERO MOLTO.Financiador: GOBIERNO DE NAVARRAConvocatoria: 2019 GN CentrosFecha de inicio: 01-02-2019Fecha fin: 30-11-2019Importe concedido: 45.552,13€Otros fondos: -
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Título: Hacia la generación de xeno-órganos mediante complementación de blastocisto (XenoOrgan)Código de expediente: RTI2018-094485-B-I00Investigador principal: XABIER ARANGUREN LOPEZ.Financiador: MINISTERIO DE CIENCIA E INNOVACIÓNConvocatoria: 2018 - PROYECTOS DE I+D RETOS INVESTIGACIONFecha de inicio: 01-01-2019Fecha fin: 30-06-2022Importe concedido: 145.200,00€Otros fondos: Fondos FEDER
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Título: Impulsando la cooperación hacia la innovación en el tratamiento de las enfermedades cardiovasculares: nuevas terapias regenerativas para el infarto de miocardioCódigo de expediente: 2019/3Investigador principal: BEATRIZ PELACHO SAMPER.Financiador: EURORREGIÓN AQUITANIA-EUSKADI-NAVARRAConvocatoria: Nueva Aquitania Euskadi Navarra 2018Fecha de inicio: 20-12-2018Fecha fin: 20-06-2020Importe concedido: 23.817,50€Otros fondos: -
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Título: Inhibidores epigenéticos e impresión 3D para lesiones tendinomusculares.Código de expediente: 0011-1383-2019-000006Investigador principal: ANA ISABEL PEREZ RUIZ.Financiador: GOBIERNO DE NAVARRAConvocatoria: 2019 - GN INDUSTRIA PROYECTOS CENTROS TECNOLOGICOS Y ORGANISMOS DE INVESTIGACIONFecha de inicio: 01-12-2018Fecha fin: 30-11-2019Importe concedido: 126.096,23€Otros fondos: -
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Título: Terapia basada en RNA mediante quimeras aptámero-siRNAs contra lncRNAs en el mieloma múltiple. RTHALMYCódigo de expediente: SAF2017-92632-EXPInvestigador principal: FELIPE LUIS PROSPER CARDOSO.Financiador: MINISTERIO DE CIENCIA E INNOVACIÓNConvocatoria: 2017 - PROYECTOS EXPLORA CIENCIA Y EXPLORA TECNOLOGIAFecha de inicio: 01-11-2018Fecha fin: 31-12-2020Importe concedido: 84.700,00€Otros fondos: Fondos FEDER
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Título: Estudio genómico para la personalización del diagnóstico y el tratamiento de los pacientes con insuficiencia cardiaca crónica y enfermedad renal crónica (Medicina cardIoreNal pERsonalizada en NaVArra) (MINERVA)Código de expediente: 0011-1411-2018-000036Investigador principal: JUAN JOSE GAVIRA GOMEZ.Financiador: GOBIERNO DE NAVARRAConvocatoria: 2018 GN PROYECTOS ESTRATEGICOS DE I+D 2018-2020Fecha de inicio: 01-04-2018Fecha fin: 30-11-2020Importe concedido: 97.237,60€Otros fondos: -
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Título: Tecnología 3D en bioingeniería de tejidos para generación de un miocardio humano maduroCódigo de expediente: 0011-1383-2018-000011Investigador principal: MANUEL MARIA MAZO VEGA.Financiador: GOBIERNO DE NAVARRAConvocatoria: 2018 - GN INDUSTRIA PROYECTOS CENTROS TECNOLOGICOS Y ORGANISMOS DE INVESTIGACIONFecha de inicio: 01-02-2018Fecha fin: 30-11-2018Importe concedido: 149.604,75€Otros fondos: -
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Título: Estudio de la arquitectura genómica y transcripcional en SMDs como herramienta para la determinación de factores pronósticos y nuevas dianas terapeúticas.Código de expediente: PI17/00701Investigador principal: FELIPE LUIS PROSPER CARDOSO.Financiador: INSTITUTO DE SALUD CARLOS IIIConvocatoria: AES2017 PROYECTOS DE INVESTIGACIÓNFecha de inicio: 01-01-2018Fecha fin: 31-12-2020Importe concedido: 209.330,00€Otros fondos: Fondos FEDER
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Título: Seudoartrois de fractura y estrés oxidativo: optimización de autoinjertos óseos miméticos y mecanismo molecular.Código de expediente: PI17/00136Investigador principal: FROILAN GRANERO MOLTO.Financiador: INSTITUTO DE SALUD CARLOS IIIConvocatoria: AES2017 PROYECTOS DE INVESTIGACIÓNFecha de inicio: 01-01-2018Fecha fin: 31-12-2020Importe concedido: 105.270,00€Otros fondos: Fondos FEDER
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Título: Desarrollo de nuevos regímenes de acondicionamiento no genotóxico para el trasplante de progenitores hematopoyéticos en hemoglobinopatías congénitas y enfermedades autoinmunes.Código de expediente: PI17/01346Investigador principal: BORJA SAEZ OCHOA.Financiador: INSTITUTO DE SALUD CARLOS IIIConvocatoria: 2017 - PROYECTOS DE I+D EN SALUDFecha de inicio: 01-01-2018Fecha fin: 31-12-2020Importe concedido: 129.470,00€Otros fondos: Fondos FEDER
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Título: ENTENDIENDO EL PAPEL DE LAS CELULAS MADRE DE PULMON EN LA REGULACION DE LA FIBROSIS PULMONAR PARA EL DESARROLLO DE NUEVAS TERAPIAS REGENERATIVAS.Código de expediente: SAF2017-89908-RInvestigador principal: ANA PARDO SAGANTA.Financiador: MINISTERIO DE CIENCIA E INNOVACIÓNConvocatoria: 2017 MINECO RETOSFecha de inicio: 01-01-2018Fecha fin: 31-12-2021Importe concedido: 171.094,00€Otros fondos: Fondos FEDER
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Título: MINECO - IJCI-2015-23390Código de expediente: IJCI-2015-23390Investigador principal: ISABEL CALVO ARNEDO.Financiador: MINISTERIO DE CIENCIA E INNOVACIÓNConvocatoria: 2015 - JUAN DE LA CIERVA INCORPORACIONFecha de inicio: 01-02-2017Fecha fin: 30-01-2018Importe concedido: 64.000,00€Otros fondos: Fondos FEDER
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Título: Red de Terapia Celular (TerCel)Código de expediente: RD16/0011/0005Investigador principal: FELIPE LUIS PROSPER CARDOSO.Financiador: INSTITUTO DE SALUD CARLOS IIIConvocatoria: 2016 AES REDESFecha de inicio: 01-01-2017Fecha fin: 30-12-2022Importe concedido: 307.285,00€Otros fondos: -
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Título: Estudio de la respuesta inmune inducida por vacunas de células dendríticas autólogas en pacientes con cáncer de mama para el desarrollo de nuevas estrategias terapéuticas.Código de expediente: PI16/01245Investigador principal: MARTA SANTISTEBAN ESLAVA, SUSANA INMACULADA INOGES SANCHO.Financiador: INSTITUTO DE SALUD CARLOS IIIConvocatoria: 2016 AES PROYECTOS DE INVESTIGACIÓNFecha de inicio: 01-01-2017Fecha fin: 31-12-2019Importe concedido: 96.800,00€Otros fondos: Fondos FEDER
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Título: Inducción de Tolerancia con células dendríticas tratadas con vitamina d3 y cargadas de mielina, en pacientes con esclerosis múltiple.Código de expediente: PI16/01797Investigador principal: ASCENSION LOPEZ DIAZ DE CERIO.Financiador: INSTITUTO DE SALUD CARLOS IIIConvocatoria: 2016 AES PROYECTOS DE INVESTIGACIÓNFecha de inicio: 01-01-2017Fecha fin: 31-12-2019Importe concedido: 55.055,00€Otros fondos: Fondos FEDER
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Título: Tratamiento del infarto de miocardio y prevención del remodelado adverso mediante la aplicación de factores de crecimiento y microRNAs anti-fibróticosCódigo de expediente: PI16/00129Investigador principal: BEATRIZ PELACHO SAMPER, JUAN JOSE GAVIRA GOMEZ.Financiador: INSTITUTO DE SALUD CARLOS IIIConvocatoria: 2016 - PROYECTOS DE I+D EN SALUDFecha de inicio: 01-01-2017Fecha fin: 30-06-2020Importe concedido: 98.615,00€Otros fondos: Fondos FEDER
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Título: Potencial de la edición génica in vivo mediante CRISPR/Cas para el tratamiento y modelado de Hiperoxaluria PrimariaCódigo de expediente: PI16/00150Investigador principal: JUAN ROBERTO RODRIGUEZ MADOZ.Financiador: INSTITUTO DE SALUD CARLOS IIIConvocatoria: 2016 - PROYECTOS DE I+D EN SALUDFecha de inicio: 01-01-2017Fecha fin: 31-12-2020Importe concedido: 80.465,00€Otros fondos: Fondos FEDER
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Título: UTILIZACIÓN DE MEMBRANAS DE COLÁGENO COMO MATRICES PARA REGENERACIÓN DE TEJIDOSCódigo de expediente: 0011-1408-2016-000003Investigador principal: IÑIGO PEREZ ESTENAGA.Financiador: GOBIERNO DE NAVARRAConvocatoria: 2016 -GN DOCTORANDOS INDUSTRIALES 2017- 2019Fecha de inicio: 01-01-2017Fecha fin: 31-12-2019Importe concedido: 85.012,50€Otros fondos: -
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Título: Estudio del potencial de los progenitores cardiovasculares inducidos en modelos de infarto de miocardio.Código de expediente: SAF2016-79398-RInvestigador principal: XONIA CARVAJAL VERGARA.Financiador: MINISTERIO DE CIENCIA E INNOVACIÓNConvocatoria: 2016 - PROYECTOS DE I+D RETOSFecha de inicio: 30-12-2016Fecha fin: 29-04-2020Importe concedido: 157.300,00€Otros fondos: Fondos FEDER
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Título: Understanding the role of lung stem cells in pulmonary fibrosisCódigo de expediente:Investigador principal: ANA PARDO SAGANTA.Financiador: GOBIERNO DE NAVARRA. DEPARTAMENTO DE SALUDConvocatoria: 2016 PROYECTOS DE I+D EN SALUDFecha de inicio: 09-12-2016Fecha fin: 08-12-2019Importe concedido: 64.316,05€Otros fondos: Fondos FEDER
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Título: POTENCIAL DE LA EDICIÓN GÉNICA IN VIVO MEDIANTE CRISPR/Cas PARA EL TRATAMIENTO DE HIPEROXALURIA PRIMARIACódigo de expediente:Investigador principal: JUAN ROBERTO RODRIGUEZ MADOZ.Financiador: GOBIERNO DE NAVARRA. DEPARTAMENTO DE SALUDConvocatoria: 2016 PROYECTOS DE I+D EN SALUDFecha de inicio: 09-12-2016Fecha fin: 08-12-2019Importe concedido: 54.964,25€Otros fondos: Fondos FEDER
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Título: MINECO RYC-2015-17233Código de expediente: RYC-2015-17233Investigador principal: XABIER ARANGUREN LOPEZ.Financiador: MINISTERIO DE CIENCIA E INNOVACIÓNConvocatoria: 2015 - MINECO RAMON Y CAJAL FIMA 2022 MINECO I3 2015 - MINECO RAMON Y CAJALFecha de inicio: 01-12-2016Fecha fin: 03-06-2024Importe concedido: 322.549,92€Otros fondos: Fondos FEDER
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Título: MINECO RYC-2015-18580Código de expediente: RYC-2015-18580Investigador principal: ANA PARDO SAGANTA.Financiador: MINISTERIO DE CIENCIA E INNOVACIÓNConvocatoria: 2015 - MINECO RAMON Y CAJALFecha de inicio: 01-12-2016Fecha fin: 22-03-2022Importe concedido: 208.600,00€Otros fondos: Fondos FEDER
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Título: Nanopartículas de esqualeno-adenosina para el tratamiento de la isquemia-reperfusión cardiacaCódigo de expediente: PCIN-2016-046Investigador principal: MARIA JOSE BLANCO PRIETO.Financiador: MINISTERIO DE CIENCIA E INNOVACIÓNConvocatoria: 2016 MINECO ACCIONES DE PROGRAMACIÓN CONJUNTA INTERNACIONALFecha de inicio: 01-05-2016Fecha fin: 31-12-2020Importe concedido: 98.000,00€Otros fondos: -
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Título: Desarrollo clínico de una terapia celular para reparación cardíaca basada en ingeniería de tejidos-CARDIOMESHCódigo de expediente: RTC-2016-4911-1Investigador principal: FELIPE LUIS PROSPER CARDOSO.Financiador: MINISTERIO DE CIENCIA E INNOVACIÓNConvocatoria: 2016 MINECO RETOS-COLABORACIONFecha de inicio: 09-03-2016Fecha fin: 28-02-2019Importe concedido: 222.982,00€Otros fondos: -
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Título: CONTRATO MIGUEL SERVET TIPO II Beatriz pelachoCódigo de expediente: MSII15/00017Investigador principal: BEATRIZ PELACHO SAMPER.Financiador: INSTITUTO DE SALUD CARLOS IIIConvocatoria: 2015 CONTRATOS DE ESTABILIZACION DE DOCTORES MIGUEL SERVET TIPO IIFecha de inicio: 01-03-2016Fecha fin: 31-01-2019Importe concedido: 87.750,00€Otros fondos: Fondos FEDER
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Título: Understanding primary hyperoxaluria type 1 towards the development of innovative therapeutic strategies (ERARE)Código de expediente: AC15/00036Investigador principal: FELIPE LUIS PROSPER CARDOSO.Financiador: INSTITUTO DE SALUD CARLOS IIIConvocatoria: 2015 AES ACCIONES COMPLEMENTARIASFecha de inicio: 01-01-2016Fecha fin: 31-12-2019Importe concedido: 99.946,00€Otros fondos: -
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Título: Biomateriales y nanopartículas para la aplicación y liberación de células y proteínas terapéuticas para la reparación del corazón (EURONANOMED-036)Código de expediente: AC15/00050Investigador principal: FELIPE LUIS PROSPER CARDOSO, FELIPE LUIS PROSPER CARDOSO.Financiador: INSTITUTO DE SALUD CARLOS IIIConvocatoria: 2015 AES ACCIONES COMPLEMENTARIASFecha de inicio: 01-01-2016Fecha fin: 30-06-2019Importe concedido: 149.435,00€Otros fondos: -
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Título: Endotelización inter-especies como estrategia para la realización de XenotrasplantesCódigo de expediente: SAF2015-064224-RInvestigador principal: XABIER ARANGUREN LOPEZ.Financiador: MINISTERIO DE CIENCIA E INNOVACIÓNConvocatoria: 2015 - PROYECTOS DE I+D RETOSFecha de inicio: 01-01-2016Fecha fin: 30-06-2019Importe concedido: 116.800,00€Otros fondos: Fondos FEDER
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Título: Endotelizacion inter-especies como estrategia para la realizacion de Xenotrasplantes (IntereXt)Código de expediente: 31/2015Investigador principal: XABIER ARANGUREN LOPEZ.Financiador: GOBIERNO DE NAVARRA. DEPARTAMENTO DE SALUDConvocatoria: 2015 PROYECTOS DE I+D EN SALUDFecha de inicio: 06-12-2015Fecha fin: 05-12-2018Importe concedido: 41.760,00€Otros fondos: Fondos FEDER
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Título: Nuevas dianas epigenáticas en mieloma múltipleCódigo de expediente: FPU2014-04331Investigador principal: RAQUEL ORDOÑEZ CIRIZA.Financiador: MINISTERIO DE CIENCIA E INNOVACIÓNConvocatoria: 2014 - MINECO BECAS FPUFecha de inicio: 01-10-2015Fecha fin: 30-09-2018Importe concedido: 59.200,00€Otros fondos: Fondos FEDER
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Título: Reprogramación cardíaca in vitro e in vivo por factores definidos como estrategia de regeneración cardíacaCódigo de expediente: BES2014-069226Investigador principal: JAVIER LINARES ACOSTA.Financiador: MINISTERIO DE CIENCIA E INNOVACIÓNConvocatoria: 2013 - MINECO FPIFecha de inicio: 24-03-2015Fecha fin: 23-03-2019Importe concedido: 83.900,00€Otros fondos: Fondos FEDER
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Título: Inhibición de la actividad metiltransferasa de G9a mediante moléculas pequeñas como estrategia terapéutica en tumores hematológicosCódigo de expediente: PI14/01867Investigador principal: FELIPE LUIS PROSPER CARDOSO.Financiador: INSTITUTO DE SALUD CARLOS IIIConvocatoria: 2014 - PROYECTOS DE I+D EN SALUDFecha de inicio: 01-01-2015Fecha fin: 30-06-2018Importe concedido: 207.515,00€Otros fondos: Fondos FEDER
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Título: Ramón y Cajal Convocatoria 2012Código de expediente: RYC-2012-10981Investigador principal: XONIA CARVAJAL VERGARA.Financiador: MINISTERIO DE CIENCIA E INNOVACIÓNConvocatoria: 2012 - MINECO RAMON Y CAJALFecha de inicio: 04-11-2013Fecha fin: 11-08-2019Importe concedido: 208.600,00€Otros fondos: Fondos FEDER
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Título: T2EVOVLE - Accelerating Development and Improving Access to CAR and TCRCódigo de expediente:Investigador principal: FELIPE LUIS PROSPER CARDOSOFinanciador: COMISIÓN EUROPEAConvocatoria: H2020-JTI-IMI2-2019-18Fecha de inicio: 01-01-2021Fecha fin: 31-12-2025Importe concedido: 271.370,00€Otros fondos: -
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Título: Red de Excelencia para el desarrollo de Terapias Avanzadas de tratamiento del Infarto de Miocardio basadas en medicina regenerativa e impresión 3DCódigo de expediente: SOE4/P1/E0163Investigador principal: BEATRIZ PELACHO SAMPERFinanciador: MINISTERIO DE HACIENDAConvocatoria: SUDOE 4/P1Fecha de inicio: 01-09-2020Fecha fin: 30-04-2023Importe concedido: 123.750,00€Otros fondos: -
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Título: Red de Excelencia para el desarrollo de Terapias Avanzadas de tratamiento del Infarto de Miocardio basadas en medicina regenerativa e impresión 3DCódigo de expediente: SOE4/P1/E1063Investigador principal: FELIPE LUIS PROSPER CARDOSOFinanciador: INTERREG SUDOEConvocatoria: INTERREG SUDOE 4ª convocatoriaFecha de inicio: 01-09-2020Fecha fin: 30-04-2023Importe concedido: 150.000,00€Otros fondos: Fondos FEDER
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Título: HEALIKICK - A modular strategy for the repair of critical sized bone fracturesCódigo de expediente: 874889Investigador principal: FROILAN GRANERO MOLTOFinanciador: COMISIÓN EUROPEAConvocatoria: SC1-BHC-07-2019: Regenerative medicine: from new insights to new applicationsFecha de inicio: 01-06-2020Fecha fin: 31-05-2025Importe concedido: 569.375,00€Otros fondos: -
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Título: MEPHOS - Shaping the Mechano-Pharmacological properties of Microparticles and Extracellular Vesicles for the Treatment of OsteoarthritisCódigo de expediente:Investigador principal: FELIPE LUIS PROSPER CARDOSOFinanciador: COMISIÓN EUROPEAConvocatoria: H2020-MSCA-RISE-2019Fecha de inicio: 01-04-2020Fecha fin: 31-03-2024Importe concedido: 257.600,00€Otros fondos: -
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Título: BRAV3: Computational biomechanics and bioengineering 3D printing to develop a personalized regenerative biological ventricular assist device to provide lasting functional support to damaged heartsCódigo de expediente: 874827Investigador principal: FELIPE LUIS PROSPER CARDOSOFinanciador: COMISIÓN EUROPEAConvocatoria: SC1-BHC-07-2019: Regenerative medicine: from new insights to new applicationsFecha de inicio: 01-01-2020Fecha fin: 31-12-2024Importe concedido: 800.500,00€Otros fondos: -
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Título: LGMed: La tecnología a servicio de la salud: desarrollo de dispositivos médicos de última generaciónCódigo de expediente: EFA313/19Investigador principal: FELIPE LUIS PROSPER CARDOSOFinanciador: POCTEFAConvocatoria: 3ª convocatoria de proyectos POCTEFA 2014-2020Fecha de inicio: 01-11-2019Fecha fin: 31-05-2022Importe concedido: 144.469,00€Otros fondos: Fondos FEDER
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Título: EHA Research Mobility Grant Alvaro Sanchez HerrerosCódigo de expediente:Investigador principal: ALVARO SANCHEZ HERREROFinanciador: European Hematology Association (EHA)Convocatoria: EHA Research Mobility Grants 2018Fecha de inicio: 12-12-2018Fecha fin: 11-03-2019Importe concedido: 6.660,00€Otros fondos: -
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Título: Early detection and intervention: Understanding the mechanisms of transformation and hidden resistance of incurable haematological malignanciesCódigo de expediente: C355/A26819Investigador principal: JESUS FERNANDO SAN MIGUEL IZQUIERDOFinanciador: ASOCIACION ESPAÑOLA CONTRA EL CANCERConvocatoria: Accelerator Grant 2017Fecha de inicio: 01-12-2018Fecha fin: 30-11-2023Importe concedido: 764.889,66€Otros fondos: -
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Título: RESTORE - Neuronal Self-Renewal by antigen-specific Tolerization in Multiple Sclerosis reinstalling the balance between inflamation and regenerationCódigo de expediente:Investigador principal: FELIPE LUIS PROSPER CARDOSOFinanciador: COMISIÓN EUROPEAConvocatoria: H2020-SC1-2017Fecha de inicio: 01-01-2018Fecha fin: 31-12-2023Importe concedido: 625.000,00€Otros fondos: -
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Título: Groundbreaking therapies and disease models for Primary HyperoxaluriaCódigo de expediente:Investigador principal: JUAN ROBERTO RODRIGUEZ MADOZFinanciador: Oxalosis & Hyperoxaluria FoundationConvocatoria: OHF 2016Fecha de inicio: 01-10-2017Fecha fin: 30-09-2019Importe concedido: 160.000,00€Otros fondos: -
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Título: REgenerative therapy of intervertebral disc: a double blind phase 2b trial of intradiscal injection of mesenchymal stromal cells in degenerative disc disease unresponsive to conventional therapy.Código de expediente:Investigador principal: FELIPE LUIS PROSPER CARDOSOFinanciador: COMISIÓN EUROPEAConvocatoria: H2020-EC-SC1-PM-11-2016Fecha de inicio: 01-01-2017Fecha fin: 31-12-2022Importe concedido: 373.000,00€Otros fondos: -
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Título: PROmuscaging. Role of proteases in muscular homeostasis and agingCódigo de expediente: 19639Investigador principal: ANA ISABEL PEREZ RUIZFinanciador: AFM TELETHONConvocatoria: Research GrantFecha de inicio: 29-04-2016Fecha fin: 29-04-2019Importe concedido: 60.310,00€Otros fondos: -
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Título: NanoReHeart: MINECO PCIN-2015-200-C02-02 Biomateriales y nanopartículas para mejorar el implante celular y liberación de factores terapéuticos para la regeneración del corazónCódigo de expediente: PCIN-2015-200-C02-02Investigador principal: BEATRIZ PELACHO SAMPERFinanciador: MINISTERIO DE CIENCIA E INNOVACIÓNConvocatoria: EURONANOMED2Fecha de inicio: 01-09-2015Fecha fin: 31-03-2019Importe concedido: 75.000,00€Otros fondos: Fondos FEDER
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Título: Identification of the epigenomic and transcriptomic alterations in the transformation of benign monoclonal gammapathies to symptomatic multiple myeloma.Investigador principal: FELIPE LUIS PROSPER CARDOSOFinanciador: FUNDACION BBVAConvocatoria: 2021 Fundación BBVA Proyectos de investigaciónFecha de inicio: 01-07-2022Fecha fin: 30-06-2024Importe concedido: 149.984,50€
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Título: Gene Regulatory NETworks in NORmal and MALignant Hematopoiesis- Identification and Targeting (GR-NET NORMAL-HITInvestigador principal: FELIPE LUIS PROSPER CARDOSOFinanciador: FUNDACIÓN BANCARIA LA CAIXAConvocatoria: 2020 FD La Caixa Health ResearchFecha de inicio: 01-12-2020Fecha fin: 30-11-2024Importe concedido: 411.250,00€
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Título: Combinatorial Immunotherapies in a novel GEMM platform for sarcomas: Identification of Therapeutic Efficacy and anticipating Adverse EventsInvestigador principal: FERNANDO LECANDA CORDEROFinanciador: ASOCIACION ESPAÑOLA CONTRA EL CANCERConvocatoria: FIMA 2020 Estratégicos AECCFecha de inicio: 01-11-2020Fecha fin: 29-02-2024Importe concedido: 300.000,00€
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Título: Desarrollo en micro-bioingeniería humana para detectar y analizar cardiotoxicidad en tratamiento anti-tumoralInvestigador principal: MANUEL MARIA MAZO VEGAFinanciador: ASOCIACION ESPAÑOLA CONTRA EL CANCERConvocatoria: FIMA Ideas Semilla 2020Fecha de inicio: 01-10-2020Fecha fin: 30-09-2022Importe concedido: 9.700,00€
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Título: Fabricación Pei 15-103 para NOMAInvestigador principal: ENRIQUE JOSE ANDREU OLTRAFecha de inicio: 17-04-2020Fecha fin: 17-04-2023Importe: 0Otros fondos: -
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Título: A systems biology approach to reveal the niche composition and connectivity in aging and malignant transformation at the single cell levelInvestigador principal: ITZIAR CENZANO ARMENDARIZFinanciador: ASOCIACION ESPAÑOLA CONTRA EL CANCERConvocatoria: FIMA 2019 Predoctorales AECC, FIMA 2019 Predoctorales AECCFecha de inicio: 01-12-2019Fecha fin: 30-11-2023Importe concedido: 91.530,54€
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Título: Making efficient cells to improve cell therapy transfer for Duchenne muscular dystrophyInvestigador principal: ANA ISABEL PEREZ RUIZFinanciador: ASOCIACION DUCHENNE PARENT PROJECTConvocatoria: III Convocatoria de Ayudas a Proyectos de Investigación Duchenne España 2018Fecha de inicio: 07-11-2018Fecha fin: 06-11-2020Importe concedido: 48.000,00€
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Título: Understanding the interactions between Acute Myeloid Leukemia and their bone marrow niche cellsInvestigador principal: BORJA SAEZ OCHOAFinanciador: ASOCIACION ESPAÑOLA CONTRA EL CANCERConvocatoria: 2016 Ayudas para investigadores en oncología, 2016 Ayudas para investigadores en oncologíaFecha de inicio: 01-09-2016Fecha fin: 30-09-2021Importe concedido: 180.000,00€
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Título: Platelage, analisis mediante citometríaInvestigador principal: FELIPE LUIS PROSPER CARDOSOFecha de inicio: 26-04-2016Fecha fin: 09-04-2019Importe: 0Otros fondos: -