A5076278258- Pulmonary Hypertension Research and Treatments
- Chronic Lymphocytic Leukemia Research
- Cardiovascular Effects of Exercise
- Cardiovascular Function and Risk Factors
- PI3K/AKT/mTOR signaling in cancer
- Genetic Syndromes and Imprinting
- Glycosylation and Glycoproteins Research
- Lymphoma Diagnosis and Treatment
- Cardiac Fibrosis and Remodeling
- Cytokine Signaling Pathways and Interactions
- Cell Adhesion Molecules Research
- Macrophage Migration Inhibitory Factor
- Immunodeficiency and Autoimmune Disorders
- Cardiac Valve Diseases and Treatments
- Coronary Interventions and Diagnostics
- Nuclear Receptors and Signaling
- Cerebrovascular and Carotid Artery Diseases
- Angiogenesis and VEGF in Cancer
- Cardiac Structural Anomalies and Repair
- Hematopoietic Stem Cell Transplantation
- Genetic and Kidney Cyst Diseases
- Peptidase Inhibition and Analysis
- Cancer Cells and Metastasis
- Epigenetics and DNA Methylation
- Monoclonal and Polyclonal Antibodies Research
Stanford University
2019-2023
University of Freiburg
2020-2022
Pulmonary and Critical Care Associates
2021
Stanford Medicine
2020
Immunité et Cancer
2017
University of Sheffield
2016
Insigneo
2016
Pulmonary arterial hypertension (PAH) is characterized by progressive narrowing of pulmonary arteries, resulting in right heart failure and death. BMPR2 (bone morphogenetic protein receptor type 2) mutations account for most familial PAH forms whereas reduced present many idiopathic forms, suggesting dysfunctional signaling to be a key feature PAH. Modulating therapeutically promising, yet how downregulated unclear.We intended identify pharmaceutically target modifier genes improve PAH.We...
Stent deployment causes endothelial cells (EC) denudation, which promotes in-stent restenosis and thrombosis. Thus regrowth in stented arteries is an important therapeutic goal. struts modify local hemodynamics, however the effects of flow perturbation on EC injury repair are incompletely understood. By studying stent migration, we identified intervention that arteries.In vitro vivo models were developed to monitor endothelialization under influence struts. A 2D parallel-plate chamber with...
The temporal sequence of events underlying functional right ventricular (RV) recovery after improvement pulmonary hypertension-associated pressure overload is unknown. We sought to establish a novel mouse model gradual RV from and use it delineate reverse-remodelling events.
Right ventricular (RV) function is the predominant determinant of survival in patients with pulmonary arterial hypertension (PAH). In preclinical models, pharmacological activation BMP (bone morphogenetic protein) signaling FK506 (tacrolimus) improved RV by decreasing afterload. therapy further stabilized three end-stage PAH. Whether has direct effects on pressure-overloaded right ventricle yet unknown. We hypothesized that increasing cardiac improves structure and a model fixed afterload...