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Research group: The candidate will join the Laboratory of Atherothrombosis at the Program of Cardiovascular Diseases, a multidisciplinary research group including clinical and basic scientists. The group has an extensive experience in vascular pathologies and thrombosis, always combining clinical and basic research. The supervisor, Dr. Carmen Roncal, has contributed to more than 40 research articles, and the group has been involved in more than 30 national and international research projects. 

Research project: Peripheral artery disease (PAD) is one of the most prevalent cardiovascular (CV) condition globally with >200 million cases. Among PAD patients, those with concomitant diabetes mellitus progress faster, and more frequently advance to critical limb ischemia, boosting their risk of thrombosis, amputation and death (2 to 3-fold) compared to non-diabetic PAD subjects. Diabetes-induced endothelial dysfunction and platelet activation play a critical role in atherothrombosis, and thus the study of the molecular changes induced by hyperglycemia on those cell types might be useful to identify novel diagnosis and prognosis biomarkers in diabetic PAD patients. Nevertheless, the inaccessibility and diffuse nature of endothelial cells hinders the possibility of studying them. In this regard, Extracellular vesicles (EVs), nanometric lipidic spheres released into blood by most cell types carrying nucleic acids, proteins and lipids from parental cells, offer a unique opportunity to analyse the content of parental cells in the bloodstream. 

The aim of this translational projects is to identify endothelial and platelet associated molecular patterns in diabetic PAD patients that will provide novel CV risk biomarkers and therapeutic targets for this high cardiovascular risk subgroup. To address our purpose, we will isolate and sequence endothelial and platelet derived EVs from diabetic and non-diabetic PAD patient, select 3 to 5 differentially expressed genes, and measure their blood levels to determine their association with worse outcome in PAD (diabetic and non-diabetic) patients. The regulation of the selected candidates by hyperglycemia will be studied in vitro and in vivo in endothelial cells, and mice models of diabetes and atherosclerosis. Finally, machine learning methods will be applied to calculate algorithms that might further improve the diagnosis and risk stratification of diabetic PAD patients.

Candidate description: We look for a highly motivated Master degree candidate, with excellent records, who is expected to enroll in a PhD programme at the Universidad de Navarra and to apply for PhD funding.

The candidate will join a research group focused in translational studies, that benefits from the experience of clinicians as well as molecular and cellular biologist with broad experience in the physiopathology of atherosclerosis and thrombosis. The candidate will receive training in cellular and molecular biology, always maintaining the focus on the translation nature of the project. He/she will participate in weekly laboratory meetings, and the advances of the project will be presented in lab seminars and national and international congresses. The candidate will be encouraged for a short-term stage abroad.

A bachelor and a master in Biomedical Sciences (e.g. biology, biochemistry, pharmacy, medicine, biomedicine…) is required. The fellow must be fluent in English (both oral and written). Previous experience in histology, cellular and molecular biology, and statistics is recommended but not essential.

Interested applicants should send a cover letter describing past experience and interests as well as their CV to: Carmen Roncal Mancho, croncalm@unav.es

Date of publication: 09/20/2021

Project title: Understanding How the Endogenous Retroelement Activation by Epigenetic Therapy Reverses the Warburg Effect and Elicits Mitochondrial-Mediated Cancer Cell Death.

Project director:  Dr. José A. Martínez-Climent

Purpose of the position: A position is offered in the Laboratory of Lymphoproliferative Syndromes of the Department of Hemato-Oncology at Cima Universidad de Navarra for the development of doctoral studies and doctoral thesis.
Required Degree: Degree in Pharmacy or Biology, and Master's degree in a cancer biology-related field.

Number of positions available: 1

Contract amount: 16.392,26 € (gross amount)

Funding entity: Cima Universidad de Navarra

Place and deadline for submitting the application: 

The information to formalize the applications for participation in this Grant Program can be found at the following link.

Applications will be sent by email to investigacion@unav.es within 15 days from the publication of this specific call.

Characteristics of the aid and other conditions of the Program:

It will be in accordance with the provisions of the Framework Call for grants attached to research projects for pre-doctoral contracts included in the following link.

For further information, we are at your disposal at the following e-mail address: investigacion@unav.es
or at telephone number 948425600 (802247).

Date of publication: 09/02/2021

Project title: ABIRES: Elucidating response to Abiraterone in metastatic castrate resistant prostate cancer

Project directors:  Prof. Mikel Hernaez and Liewei Wang

Purpose of the position: Development of the doctoral thesis in the context of the PROMOTE project, in collaboration with the Mayo Clinic, USA. The candidate will develop computational tools using artificial intelligence to elucidate transcriptomic changes between responders and non-responders to the drug ABIRATERONE in patients with metastatic castration-resistant prostate cancer.
Required Degree: Advanced degree in Pharmacy/Biochemistry/Telecommunications/Mathematics/ or similar. Master's degree in computational methods/Machine Learning or similar is required.

Number of positions available: 1

Contract amount: 20,775,88 € (including SS payable by the entity and insurance).

Funding entity: US Department of Defense

Place and deadline for submitting the application: 

The information to formalize the applications for participation in this Grant Program can be found at the following link.

Applications will be sent by email to investigacion@unav.es within 15 days from the publication of this specific call.

Characteristics of the aid and other conditions of the Program:

It will be in accordance with the provisions of the Framework Call for grants attached to research projects for pre-doctoral contracts included in the following link.

For further information, we are at your disposal at the following e-mail address: investigacion@unav.es
or at telephone number 948425600 (802247).

Date of publication: 08/16/2021

Project title: Local Immunotherapy (LIRT)
 

Project director: Prof. Ignacio Melero Bermejo

Number of positions available: 1

Contract amount: 20,666,25 € (including SS payable by the entity and insurance).

Funding entity: Asociación Española contra el Cáncer (AECC)

Place and deadline for submitting the application: 

The information to formalize the applications for participation in this Grant Program can be found at the following link.

Applications will be sent by email to investigacion@unav.es within 15 days from the publication of this specific call.

Characteristics of the aid and other conditions of the Program:

It will be in accordance with the provisions of the Framework Call for grants attached to research projects for pre-doctoral contracts included in the following link.

For further information, we are at your disposal at the following e-mail address: investigacion@unav.es
or at telephone number 948425600 (802247).

Date of publication: 08/16/2021

A lab technician position, supported by “la Caixa Research”, is available in the group headed by Maite Huarte at Cima Universidad de Navarra, in Pamplona, Spain.

The candidate will work with a multidisciplinary team to support research that aims to understand the role of lncRNAs in genomic stability and cancer

The position offers the opportunity for professional growth by working in an interactive and dynamic international environment of translational and basic science research. 

  • We are looking for highly motivated and talented individuals, with previous experience in molecular and cellular biology.
  • Knowledge of NGS techniques, including library generation and data interpretation are highly valued.

Interested applicants should send a cover letter describing their past experience and interests, as well as their CV (including Educational Information and scores as well as references) to Maite Huarte, maitehuarte@unav.es. T + 34 948 194 700 ext 814000

Our laboratory at Cima Universidad de Navarra, in Spain, is recruiting a highly motivated lab technician/postdoc to work on long noncoding RNAs and cancer genomics.

The position is founded by the Government of Navarra and offers the opportunity to work in a collaborative project with a multidisciplinary team of clinical, translational and basic researchers.   

  • Previous experience in RNA, genomics, molecular biology and biochemistry, are required.
  • The familiarity with the preparation of libraries for next generation sequencing will be very positively valued.
  • Experience with processing of human samples and knowledge of bioinformatics will also be considered. 

Interested applicants should send their CV including references to Puri Fortes, pfortes@unav.es T + 34 948 194 700 ext 814025 and/or Maite Huarte, maitehuarte@unav.es. T + 34 948 194 700 ext 814000

Project title:

 An integrative omics approach to characterize the human bone marrow microenvironment in plasma cell dyscrasias: description of new therapeutic vulnerabilities in MGUS and Multipl Myeloma.

Project director: José Juan Rifón Roca and Borja Sáez Ochoa.

Number of positions available: 1

Contract amount: 20,775.88 € (including SS payable by the entity and insurance).

Funding entity: Fundación AECC (Accelerator Award)

Place and deadline for submitting the application: 

The information to formalize the applications for participation in this Grant Program can be found at the following link.

Applications will be sent by email to investigacion@unav.es within 15 days from the publication of this specific call.

Characteristics of the aid and other conditions of the Program:

It will be in accordance with the provisions of the Framework Call for grants attached to research projects for pre-doctoral contracts included in the following link.

For further information, we are at your disposal at the following e-mail address: investigacion@unav.es
or at telephone number 948425600 (802247).

A postdoctoral position supported by “la Caixa Research” is available in the group headed by Maite Huarte at Cima Universidad de Navarra, in Pamplona, Spain.

  • The candidate will work on a collaborative project with a multidisciplinary team of molecular, structural, computational and biophysics experts to understand the role of lncRNAs in the response to replicative stress in cancer cells.
  • We are looking for highly motivated and talented individuals, preferentially with previous expertise in molecular, RNA, chromatin and cancer biology.
  • Knowledge of the analysis and interpretation of genomic data are desirable.

The position offers the opportunity for professional growth by working in an interactive and dynamic international environment of translational and basic science research.
 

Interested applicants should send a cover letter describing their past experience and interests, as well as their CV (including Educational Information and scores as well as references) to: Maite Huarte, maitehuarte@unav.es. T + 34 948 194 700 ext 814000

PI: Begoña Salazar

Diffuse myocardial fibrosis, or exaggerated accumulation of collagen in the myocardium, plays a key role in the development and progression of chronic heart failure. The enzymatic systems involved in the processing of collagen fibers emerge as key mechanisms of the process.

In this regard, 2 relevant systems have recently been identified in the axis of the formation of mature collagen fibers: 1) carboxy-terminal procollagen proteinase (PCP) with its enhancer PCPE-1, which processes the passage from immature procollagen to collagen capable of forming fibers; and 2) lysyl oxidase (LOX), the main enzyme responsible for collagen cross-linking, a process that facilitates the formation of collagen fibers and their deposition.

In recent years it has been shown that myocardial fibrosis is characterized not only by an increase in the quantity of collagen but also by alterations in its quality, such as an increase in the degree of collagen cross-linking (GrE).

This process, as already mentioned, is mainly mediated by enzymes of the lysyl oxidase (LOX) family, and leads to the formation of insoluble collagen fibers that are stiffer and more resistant to degradation.

Patients with a malignant fibrosis phenotype characterized by severe deposition of highly cross-linked collagen fibers have an increased risk of hospitalization or death from cardiovascular causes, as well as an increased risk of complications associated with heart failure such as atrial fibrillation.

Objectives

  1. To deepen in the impact of the different myocardial fibrosis phenotypes in the development and evolution of chronic heart failure and its associated pathologies in patients with heart failure at different stages of evolution and in experimental models (animals and cell cultures).
  2. To analyze the relevance of collagen synthesis (PCP/PCPE-1-LOX) and degradation (matrix metalloproteinases or MMPs) systems in patients with heart failure of different etiology and in models of pressure overload.
  3. To validate the PCP/PCPE-1 system as a therapeutic target for the treatment of myocardial fibrosis in pressure overload models.
  4. To assess the impact of GrE and increased extracellular matrix stiffness on cardiac cell behavior.
  5. To identify new molecular mediators and/or biomarkers involved in the development of diffuse myocardial fibrosis.

A PhD position supported by “Agencia Estatal de Investigación” will open soon to work in the group headed by Maite Huarte at Cima Universidad de Navarra, in Pamplona, Spain.
Our lab aims to understand how RNA in general and lncRNA in particular affect chromatin replication and gene regulation in cancer. By working in a stimulating environment with an international team of translational and basic researchers, the position offers the opportunity of being trained in the latest technologies for the study of non-coding genes, ranging from molecular and cellular biology to epigenetics and functional genomics.
Please visit our lab webpage.

  • We are looking for candidates with an interest in applying to this PhD call, likely to open sometime after the summer, bearing in mind that the call will impose formal requirement for applicants. Salaries and other conditions will be defined.
  • We look for highly motivated individuals with a science/master’s degree.
  • Some experience in molecular and cellular biology is highly recommended and background in biology positively valued.
  • Excellent knowledge of the English language is required.

Interested applicants should send a cover letter describing their past experience and interests as well as their CV (including Educational Information and scores as well as references) to: Maite Huarte, maitehuarte@unav.es. T + 34 948 194 700 ext 814000

A postdoctoral position is offered at the OnTarget Group led by professor Silve Vicent at the Center for Applied Medical Research (Cima University of Navarra). The project is aimed at the identification of new oncogenic vulnerabilities and therapeutic strategies for the treatment of tumors with KRAS mutations (Vallejo et al, J Hepatology 2021; Valencia et al, JCI 2020; Vallejo et al, Nat Comms 2017; Roman et al, Mol Cancer, 2018; Roman et al, Cancer Res., 2018) and will provide opportunities for interaction with other groups (internally, nationally and internationally) as well as industry partners.

The project will require, among other tasks: generation of new 3D tumor organoid and syngeneic models using the CRISPR/Cas9 genome editing technology, functional characterization of new elements within the KRAS network, testing of novel combinatorial therapies involving targeted therapies and immune checkpoint inhibitors, and characterization of the mechanism of action for nominated genes and/or drug combinations using high-throughput (RNAseq, scRNAseq and/or proteomics) and focused (qPCR, WB, IF and live imaging) approaches. 

Candidate’s requirements:
- PhD in biological or biomedical sciences obtained in the last 12-24 months.
- Self-motivated, autonomous person with team work skills and ability to work in various projects.
- Background in Immunotherapy and/or Cancer Biology would be ideal.
- Training in animal work would be desirable.
- Experience in data set analysis and with computational tools would be advantageous.
- Publication record to compete for additional fellowship applications (e.g. Marie Curie actions, Juan de la Cierva…) is preferable (at least one first-author publication).
The postdoctoral position is initially funded for 2 years (renewed annually) and could be extended for an additional year. The appointment will start in September 2021. Applications will be accepted starting June 25th and until the position is filled.
Interested applicants should send a cover letter describing past experience and interests, as well as their CV including at least two references to: silvevicent@unav.es
About Cima:

Cima is the biomedical research center of the Clínica Universidad de Navarra. Our scientific objective is to address current clinical problems and to propose the most effective treatment for each patient. We are a reference in cancer, heart and liver diseases, immunotherapy and gene therapy research. With our academic status, we work on a non-profit basis to reinvest the surpluses in our research and to fulfill our mission of service to patients and society. CIMA is committed to excellence in translational research, based on novel biological knowledge and aimed at finding therapeutic solutions to patients' needs. To transfer the results of basic research to clinical application, Cima’s Translation and Transfer unit seeks to establish collaborations with biotechnology and pharmaceutical companies to facilitate the arrival of scientific discoveries to the patient.

PI: Begoña Salazar

Diffuse myocardial fibrosis, or exaggerated accumulation of collagen in the myocardium, plays a key role in the development and progression of chronic heart failure. The enzymatic systems involved in the processing of collagen fibers emerge as key mechanisms of the process.

In this regard, 2 relevant systems have recently been identified in the axis of the formation of mature collagen fibers: 1) carboxy-terminal procollagen proteinase (PCP) with its enhancer PCPE-1, which processes the passage from immature procollagen to collagen capable of forming fibers; and 2) lysyl oxidase (LOX), the main enzyme responsible for collagen cross-linking, a process that facilitates the formation of collagen fibers and their deposition.

In recent years it has been shown that myocardial fibrosis is characterized not only by an increase in the quantity of collagen but also by alterations in its quality, such as an increase in the degree of collagen cross-linking (GrE).

This process, as already mentioned, is mainly mediated by enzymes of the lysyl oxidase (LOX) family, and leads to the formation of insoluble collagen fibers that are stiffer and more resistant to degradation.

Patients with a malignant fibrosis phenotype characterized by severe deposition of highly cross-linked collagen fibers have an increased risk of hospitalization or death from cardiovascular causes, as well as an increased risk of complications associated with heart failure such as atrial fibrillation.

Objectives

  1. To deepen in the impact of the different myocardial fibrosis phenotypes in the development and evolution of chronic heart failure and its associated pathologies in patients with heart failure at different stages of evolution and in experimental models (animals and cell cultures).
  2. To analyze the relevance of collagen synthesis (PCP/PCPE-1-LOX) and degradation (matrix metalloproteinases or MMPs) systems in patients with heart failure of different etiology and in models of pressure overload.
  3. To validate the PCP/PCPE-1 system as a therapeutic target for the treatment of myocardial fibrosis in pressure overload models.
  4. To assess the impact of GrE and increased extracellular matrix stiffness on cardiac cell behavior.
  5. To identify new molecular mediators and/or biomarkers involved in the development of diffuse myocardial fibrosis.

PI: Begoña Salazar

Diffuse myocardial fibrosis, or exaggerated accumulation of collagen in the myocardium, plays a key role in the development and progression of chronic heart failure. The enzymatic systems involved in the processing of collagen fibers emerge as key mechanisms of the process.

In this regard, 2 relevant systems have recently been identified in the axis of the formation of mature collagen fibers: 1) carboxy-terminal procollagen proteinase (PCP) with its enhancer PCPE-1, which processes the passage from immature procollagen to collagen capable of forming fibers; and 2) lysyl oxidase (LOX), the main enzyme responsible for collagen cross-linking, a process that facilitates the formation of collagen fibers and their deposition.

In recent years it has been shown that myocardial fibrosis is characterized not only by an increase in the quantity of collagen but also by alterations in its quality, such as an increase in the degree of collagen cross-linking (GrE).

This process, as already mentioned, is mainly mediated by enzymes of the lysyl oxidase (LOX) family, and leads to the formation of insoluble collagen fibers that are stiffer and more resistant to degradation.

Patients with a malignant fibrosis phenotype characterized by severe deposition of highly cross-linked collagen fibers have an increased risk of hospitalization or death from cardiovascular causes, as well as an increased risk of complications associated with heart failure such as atrial fibrillation.

Objectives

  1. To deepen in the impact of the different myocardial fibrosis phenotypes in the development and evolution of chronic heart failure and its associated pathologies in patients with heart failure at different stages of evolution and in experimental models (animals and cell cultures).
  2. To analyze the relevance of collagen synthesis (PCP/PCPE-1-LOX) and degradation (matrix metalloproteinases or MMPs) systems in patients with heart failure of different etiology and in models of pressure overload.
  3. To validate the PCP/PCPE-1 system as a therapeutic target for the treatment of myocardial fibrosis in pressure overload models.
  4. To assess the impact of GrE and increased extracellular matrix stiffness on cardiac cell behavior.
  5. To identify new molecular mediators and/or biomarkers involved in the development of diffuse myocardial fibrosis.

PI: Begoña Salazar

Diffuse myocardial fibrosis, or exaggerated accumulation of collagen in the myocardium, plays a key role in the development and progression of chronic heart failure. The enzymatic systems involved in the processing of collagen fibers emerge as key mechanisms of the process.

In this regard, 2 relevant systems have recently been identified in the axis of the formation of mature collagen fibers: 1) carboxy-terminal procollagen proteinase (PCP) with its enhancer PCPE-1, which processes the passage from immature procollagen to collagen capable of forming fibers; and 2) lysyl oxidase (LOX), the main enzyme responsible for collagen cross-linking, a process that facilitates the formation of collagen fibers and their deposition.

In recent years it has been shown that myocardial fibrosis is characterized not only by an increase in the quantity of collagen but also by alterations in its quality, such as an increase in the degree of collagen cross-linking (GrE).

This process, as already mentioned, is mainly mediated by enzymes of the lysyl oxidase (LOX) family, and leads to the formation of insoluble collagen fibers that are stiffer and more resistant to degradation.

Patients with a malignant fibrosis phenotype characterized by severe deposition of highly cross-linked collagen fibers have an increased risk of hospitalization or death from cardiovascular causes, as well as an increased risk of complications associated with heart failure such as atrial fibrillation.

Objectives

  1. To deepen in the impact of the different myocardial fibrosis phenotypes in the development and evolution of chronic heart failure and its associated pathologies in patients with heart failure at different stages of evolution and in experimental models (animals and cell cultures).
  2. To analyze the relevance of collagen synthesis (PCP/PCPE-1-LOX) and degradation (matrix metalloproteinases or MMPs) systems in patients with heart failure of different etiology and in models of pressure overload.
  3. To validate the PCP/PCPE-1 system as a therapeutic target for the treatment of myocardial fibrosis in pressure overload models.
  4. To assess the impact of GrE and increased extracellular matrix stiffness on cardiac cell behavior.
  5. To identify new molecular mediators and/or biomarkers involved in the development of diffuse myocardial fibrosis.

Research group: The candidate will join a multidisciplinary research group including clinical and basic scientists. The group has an extensive trajectory of more than 20 years in heart failure, focused on myocardial remodeling and the validation of blood biomarkers. The supervisor, Dr. González, has participated in 130 scientific publications and the group has been involved in over 50 research projects, including National and collaborative European Commission-funded projects (FP7, H2020, ERA-NET) and contracts with pharmaceutical companies. 

Research project: Heart failure (HF) is one of the leading causes of death and hospitalization. HF with preserved ejection fraction (HFpEF), with increasing prevalence given its association with risks factors such as hypertension, diabetes and aging, remains poorly understood and lacks specific diagnostic and therapeutic strategies. Microvascular dysfunction and the associated cardiac inflammation have been proposed as key players leading to myocardial remodeling and cardiac dysfunction in HFpEF. Of note, one of the hallmarks of myocardial remodeling in HFpEF is the development of diffuse interstitial fibrosis, which increases the stiffness of the cardiac tissue. However the pathophysiological mechanisms mediated by microvascular dysfunction, and in particular its association with fibrosis, need to be further studied. On the other hand, there is an unmet need to develop sensitive tools for the non-invasive assessment of myocardial microvascular dysfunction (by either cardiac imaging techniques or blood biomarkers). 

This translational project is focused on: 1) Understanding the contribution of microvascular dysfunction to cardiac inflammation, myocardial fibrosis and cardiac dysfunction in patients at different stages of evolution of HFpEF and in experimental models; 2) Validating novel imaging biomarkers of myocardial microvascular dysfunction by cardiac magnetic resonance; 3) Identifying novel blood biomarkers derived from endothelial cells microvesicles by next generation sequencing (mRNA-Seq).

Candidate description: The fellow is expected to enroll in a PhD programme at the Universidad de Navarra.

He/She will become a member of a leading research group, which follows a translational approach to understand the mechanisms involved in HF development, aiming at identifying new diagnostic tools and therapeutic strategies. Moreover, the project will involve interaction with international collaborators of ongoing related projects and a short term stay in a European-based research lab within the group network.

A bachelor and a master in Biomedical Sciences (e.g. biology, biochemistry, pharmacy, medicine, biomedicine…) is required. 
The fellow must be fluent in English (both oral and written). Previous experience in histology, cell biology, RNA analysis and biostatistics is recommended but not essential. 

The candidate will benefit from a multidisciplinary training to understand the pathophysiology of HFpEF and the current clinical gaps in diagnosis and management, as well as from obtaining the technical skills required. 

Interested applicants should send a cover letter describing past experience and interests as well as their CV to:
Arantxa González Miqueoamiqueo@unav.es

PI: Susana Ravassa

Chronic heart failure is a heterogeneous syndrome, the end result of diverse pathophysiological mechanisms and different histocellular alterations.

In order to design personalized therapeutic strategies aimed at correcting the predominant alterations in each patient, it is necessary to have precise biomarkers that allow early diagnosis, better risk stratification in patients and monitoring of the effects of therapy. 

Since obtaining endomyocardial biopsies is not feasible on a large scale, circulating and imaging biomarkers are a useful tool for the analysis of large patient populations. In recent years we have defined a panel of biomarkers of myocardial remodeling that includes markers of fibrosis (PICP and CITP:MMP-1), cardiomyocyte damage and stress (NT-proBNP and hs-TnT) and inflammation (IL-18, sST-2, galectin-3).

Similarly, advances in cardiac magnetic resonance have allowed the development of new parameters to assess microvascular alterations and diffuse myocardial fibrosis.

This project focuses on analyzing the diagnostic and therapeutic usefulness of the panel of biomarkers of myocardial remodeling and identifying new molecular biomarkers to define molecular profiles corresponding to the different phenotypes of patients with chronic heart failure.

Objectives

  1. To establish a profile of circulating and cardiac imaging biomarkers that reflect the different aspects of myocardial remodeling. Biomarkers already identified will be combined with new biomarkers under development, derived from proteomic studies and characterization of non-coding RNAs.
  2. To assess the diagnostic and prognostic utility of the panel of biomarkers of myocardial remodeling in patients with chronic heart failure of different etiologies and different associated pathologies (atrial fibrillation, chronic kidney disease...).
  3. To analyze the usefulness of the myocardial remodeling biomarker panel for monitoring the effects of therapy in patients with chronic heart failure and associated pathologies.
  4. To use the myocardial remodeling biomarker panel to detect cardiovascular sequelae in patients with cardiotoxicity induced by chemotherapeutic agents or in patients infected with Sars-CoV-2.

PI: Mª Ujué Moreno Zulategui

In recent years it has been demonstrated that extracellular vesicles (EVs) are actively released in response to tissue damage, so that the analysis of both their number and content can provide valuable information both in terms of the identification of new biomarkers and new pathophysiological mechanisms. In fact, it has been proposed that EVs may act as mediators by transferring their content (proteins, non-coding RNAs or mRNAs) to target cells in a paracrine or endocrine manner.

The optimization of massive sequencing technologies (NGS) for serum and plasma studies has allowed the characterization of the transcriptome of EVs present in plasma, as well as the analysis of circulating non-coding RNAs.

This approach will make it possible to establish molecular profiles associated with the different phenotypes of chronic heart failure, which may also be pathophysiological mediators, and to lay the foundations for the identification of new therapeutic targets.

Objectives

  1. To characterize the cellular origin (endothelial, platelet, cardiomyocyte, leukocyte) of plasma EVs in patients with chronic heart failure of different etiologies and at different stages of evolution.
  2. To identify new biomarkers by analyzing the transcriptome (mRNA-Seq) of plasma EVs in patients with chronic heart failure and their associated co-morbidities (chronic kidney disease, atrial fibrillation).
  3. To validate the pathophysiological relevance of targets identified in the analysis of the transcriptome of EVs in cellular and animal models.
  4. To evaluate the transcriptome of endothelial-derived EVs to assess the implication of microvascular alterations as a common causal mechanism in chronic heart failure with preserved ejection fraction and cognitive impairment.
  5. To establish new biomarkers based on the analysis of the serum microRNA-ome in patients with chronic heart failure of different etiologies and at different stages of evolution.

PI: Arantxa González Miqueo

Heart failure with preserved ejection fraction is a very heterogeneous pathology in which non-cardiac systemic co-morbidities such as hypertension, diabetes or chronic kidney disease play a key role.

Available therapies, more focused on mitigating symptoms than treating the underlying pathophysiological mechanisms, have not demonstrated a significant improvement in the prognosis of these patients.

From a mechanistic perspective, in recent years, systemic inflammation has been described as causing myocardial endothelial dysfunction, microvascular alterations and increased leukocyte infiltration, which trigger myocardial remodeling (including the development of myocardial fibrosis) and subsequent functional deterioration in patients with heart failure with preserved ejection fraction. 

These pathophysiological mechanisms are also involved in other complications associated with this syndrome that affect the brain, such as cognitive impairment or the generation of cardioembolic thrombi, which is one of the main causes of ischemic stroke.  

Therefore, this project focuses on analyzing the association between microvascular alterations, inflammation and the development of myocardial fibrosis, as well as its impact on cardiac function and the development and progression of heart failure with preserved ejection fraction.

Likewise, we seek to deepen in the pathophysiological mechanisms common with brain pathologies such as cognitive impairment or cardio-embolic thrombus formation.

Objectives

  1. To characterize microvasculature alterations, inflammation and myocardial fibrosis phenotype in patients with heart failure with preserved ejection fraction and associated cardiac pathologies (e.g. atrial fibrillation).
  2. To evaluate the contribution of endothelial dysfunction and inflammation in the development of fibrosis in cellular studies.
  3. To analyze the anti-fibrotic potential of new drugs used in the treatment of chronic heart failure (e.g. iSGLT2, finerenone...).
  4. To study the association of chronic heart failure with preserved ejection fraction and brain involvement using circulating and imaging biomarkers that reflect microvascular alterations.
  5. To evaluate the role of atrial myopathy (inflammation, endothelial dysfunction and fibrosis) in the development of cardioembolic thrombus and ischemic stroke.

PI: Arantxa González Miqueo

Heart failure with preserved ejection fraction is a very heterogeneous pathology in which non-cardiac systemic co-morbidities such as hypertension, diabetes or chronic kidney disease play a key role.

Available therapies, more focused on mitigating symptoms than treating the underlying pathophysiological mechanisms, have not demonstrated a significant improvement in the prognosis of these patients.

From a mechanistic perspective, in recent years, systemic inflammation has been described as causing myocardial endothelial dysfunction, microvascular alterations and increased leukocyte infiltration, which trigger myocardial remodeling (including the development of myocardial fibrosis) and subsequent functional deterioration in patients with heart failure with preserved ejection fraction. 

These pathophysiological mechanisms are also involved in other complications associated with this syndrome that affect the brain, such as cognitive impairment or the generation of cardioembolic thrombi, which is one of the main causes of ischemic stroke.  

Therefore, this project focuses on analyzing the association between microvascular alterations, inflammation and the development of myocardial fibrosis, as well as its impact on cardiac function and the development and progression of heart failure with preserved ejection fraction.

Likewise, we seek to deepen in the pathophysiological mechanisms common with brain pathologies such as cognitive impairment or cardio-embolic thrombus formation.

Objectives

  1. To characterize microvasculature alterations, inflammation and myocardial fibrosis phenotype in patients with heart failure with preserved ejection fraction and associated cardiac pathologies (e.g. atrial fibrillation).
  2. To evaluate the contribution of endothelial dysfunction and inflammation in the development of fibrosis in cellular studies.
  3. To analyze the anti-fibrotic potential of new drugs used in the treatment of chronic heart failure (e.g. iSGLT2, finerenone...).
  4. To study the association of chronic heart failure with preserved ejection fraction and brain involvement using circulating and imaging biomarkers that reflect microvascular alterations.
  5. To evaluate the role of atrial myopathy (inflammation, endothelial dysfunction and fibrosis) in the development of cardioembolic thrombus and ischemic stroke.

PI: Arantxa González Miqueo

Heart failure with preserved ejection fraction is a very heterogeneous pathology in which non-cardiac systemic co-morbidities such as hypertension, diabetes or chronic kidney disease play a key role.

Available therapies, more focused on mitigating symptoms than treating the underlying pathophysiological mechanisms, have not demonstrated a significant improvement in the prognosis of these patients.

From a mechanistic perspective, in recent years, systemic inflammation has been described as causing myocardial endothelial dysfunction, microvascular alterations and increased leukocyte infiltration, which trigger myocardial remodeling (including the development of myocardial fibrosis) and subsequent functional deterioration in patients with heart failure with preserved ejection fraction. 

These pathophysiological mechanisms are also involved in other complications associated with this syndrome that affect the brain, such as cognitive impairment or the generation of cardioembolic thrombi, which is one of the main causes of ischemic stroke.  

Therefore, this project focuses on analyzing the association between microvascular alterations, inflammation and the development of myocardial fibrosis, as well as its impact on cardiac function and the development and progression of heart failure with preserved ejection fraction.

Likewise, we seek to deepen in the pathophysiological mechanisms common with brain pathologies such as cognitive impairment or cardio-embolic thrombus formation.

Objectives

  1. To characterize microvasculature alterations, inflammation and myocardial fibrosis phenotype in patients with heart failure with preserved ejection fraction and associated cardiac pathologies (e.g. atrial fibrillation).
  2. To evaluate the contribution of endothelial dysfunction and inflammation in the development of fibrosis in cellular studies.
  3. To analyze the anti-fibrotic potential of new drugs used in the treatment of chronic heart failure (e.g. iSGLT2, finerenone...).
  4. To study the association of chronic heart failure with preserved ejection fraction and brain involvement using circulating and imaging biomarkers that reflect microvascular alterations.
  5. To evaluate the role of atrial myopathy (inflammation, endothelial dysfunction and fibrosis) in the development of cardioembolic thrombus and ischemic stroke.

PI: Arantxa González Miqueo

Heart failure with preserved ejection fraction is a very heterogeneous pathology in which non-cardiac systemic co-morbidities such as hypertension, diabetes or chronic kidney disease play a key role.

Available therapies, more focused on mitigating symptoms than treating the underlying pathophysiological mechanisms, have not demonstrated a significant improvement in the prognosis of these patients.

From a mechanistic perspective, in recent years, systemic inflammation has been described as causing myocardial endothelial dysfunction, microvascular alterations and increased leukocyte infiltration, which trigger myocardial remodeling (including the development of myocardial fibrosis) and subsequent functional deterioration in patients with heart failure with preserved ejection fraction. 

These pathophysiological mechanisms are also involved in other complications associated with this syndrome that affect the brain, such as cognitive impairment or the generation of cardioembolic thrombi, which is one of the main causes of ischemic stroke.  

Therefore, this project focuses on analyzing the association between microvascular alterations, inflammation and the development of myocardial fibrosis, as well as its impact on cardiac function and the development and progression of heart failure with preserved ejection fraction.

Likewise, we seek to deepen in the pathophysiological mechanisms common with brain pathologies such as cognitive impairment or cardio-embolic thrombus formation.

Objectives

  1. To characterize microvasculature alterations, inflammation and myocardial fibrosis phenotype in patients with heart failure with preserved ejection fraction and associated cardiac pathologies (e.g. atrial fibrillation).
  2. To evaluate the contribution of endothelial dysfunction and inflammation in the development of fibrosis in cellular studies.
  3. To analyze the anti-fibrotic potential of new drugs used in the treatment of chronic heart failure (e.g. iSGLT2, finerenone...).
  4. To study the association of chronic heart failure with preserved ejection fraction and brain involvement using circulating and imaging biomarkers that reflect microvascular alterations.
  5. To evaluate the role of atrial myopathy (inflammation, endothelial dysfunction and fibrosis) in the development of cardioembolic thrombus and ischemic stroke.

We are seeking for a creative, ambitious and highly motivated Postdoc candidate to join a fully funded project within the Hematology-Oncology Program at CIMA Universidad de Navarra.

The candidate will join a highly collaborative environment with the opportunity to apply cutting-edge genomic technologies on the field of Hematology Oncology. The work will be in permanent collaboration with an interactive international team of basic and translational researchers.

The successful candidate will:

  • Work in a unique team of experts in Multiple Myeloma

  • Participate in high impact projects involving next generation sequencing experiments for the study of gene regulation and epigenetics (RNA-seq, ChIP-seq, ATAC-seq, HI-C, single cell RNA-seq, etc.), flow cytometry and cellular and molecular studies.

  • Analyze and integrate cancer genomic data.

  • Participate in the development of data analysis workflows and pipelines for high throughput “omics” data.

  • Collaborate in multiple projects, having the possibility to carry on a personal research project.

  • Collaborate with the development of any bioinformatic necessary tools to accomplish goals.

  • Be involved in a project that moves from early basic research towards clinical translation and from massive studies to single molecules

  • Co-supervise PhD and Master students

  • Participate in the oral presentation of all project findings and abstracts including participation in periodic project status meetings and presentation of final project deliverables

Required qualifications:

  • PhD training in molecular and cellular biology with skills in NGS and flow cytometry techniques and/or Multiple Myeloma.

  • Experience in sample processing, cellular and molecular biology.

  • Animal handling experience.

  • Excellent interpersonal skills (project management, English and communication –oral and written-, motivation and resilience, organization, creativity, initiative, vision, connectedness, teamwork abilities…).

  • Experience with multidisciplinary approaches and bioinformatics are highly desirable. Applicants are encouraged to apply for competitive fellowship awards. Salary will be commensurate with qualifications and experience.

Interested applicants should send a cover letter describing past experience and interests as well as their CV including references to:

Oscar González
ogonmor@unav.es
T + 34 948 194 700 ext 811047

Location: Regenerative Medicine Program. CIMA, Navarra (Spain)

Contract: Technician position, full time, for 1 year and 3 months. The position is available from 11th of January 2021

Application process: applicants must send to Xabier Aranguren (xlaranguren@unav.es) a cover letter describing experience and research interests, and an up-to-date CV. 

Project scope: 

Inter-species chimera generation and transgenesis in a pig model

Candidates with the following expertises will be preferred:

  • Training in molecular and cellular biology: CRISPR/Cas9 technology, stem cell cultures
  • Animal handling experienc

Location: Gene Therapy and Regulation of Gene Expression Program. CIMA, research Center of the University of Navarra and Clínica Universidad de Navarra (CUN).

Contract: Postdoctoral position, full time, for 8 months with possibility of renewal

Application process: applicants must send to Puri Fortes (pfortes@unav.es) a cover letter describing experience and research interests, and an up-to-date CV including the name and addresses of three former mentors for reference letters.

Project scope: The position is available from November 1st, 2020 for the development of novel therapies for hepatocellular carcinoma (HCC) targeting long non-coding RNAs

The successful candidate will:

  • work in an unique team of experts in functional RNAs
  • use up-to-date models for nucleic acid delivery in vitro and in vivo
  • develop preclinical models for HCC
  • co-supervise PhD and Master students
  • be involved in a project that moves from early basic research towards clinical translation and from massive studies to single molecules
  • collaborate with basic researchers in biotechnology and functional RNAs and bioinformaticians at CIMA and with clinical researchers at CUN

Qualifications to be considered

  • PhD training in molecular and cellular biology with skills in RNA techniques and/or HCC
  • Animal handling experience
  • Excellent interpersonal skills (project management, English and communication –oral and written-, motivation and resilience, organization, creativity, initiative, vision, connectedness, teamwork abilities…)
  • Experience with multidisciplinary approaches and bioinformatics are highly desirable. Applicants are encouraged to apply for competitive fellowship awards.
  • Salary will be commensurate with qualifications and experience.

Location: Gene Therapy and Regulation of Gene Expression Program. CIMA, research Center of the University of Navarra.

Contract: Technician position, full time, for 6 months
Application process: applicants must send to Puri Fortes (pfortes@unav.es) a cover letter describing experience and research interests, and an up-to-date CV including the name and addresses of three former mentors for reference letters. 

Project scope: The position is available from November 1st, 2020 for the evaluation of gene expression in mouse models using up-to-date technology

The successful candidate will

  • Work in an unique team of experts liver cancer and functional RNAs
  • Use up-to-date models for nucleic acid delivery in vitro and in vivo
  • Be involved in a project that moves from early basic research towards clinical translation and from massive studies to single molecules
  • Collaborate with basic researchers in biotechnology and functional RNAs and bioinformaticians at CIMA and with clinical researchers at CUN

Qualifications to be considered

  • Training in molecular and cellular biology
  • Animal handling experience
  • Excellent interpersonal skills (motivation and resilience, organization, creativity, initiative, vision, connectedness, teamwork abilities…)
  • Experience with multidisciplinary approaches and bioinformatics are highly desirable. Salary will be commensurate with qualifications and experience.

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The Cima Universidad de Navarra is committed to the best professionals as a differentiating element and guarantor of this service. More than 300 professionals from different disciplines work at Cima: researchers, engineers, laboratory technicians, administrative and management personnel.... 

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If you think that your educational and professional background may fit with any of the above mentioned professional profiles or with any other of the Cima departments, do not hesitate to send us your curriculum vitae.

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