About The Lab...
The Advanced Heart Failure Research Laboratory has its roots at Stanford University (1992-1993), evolved at Muenster University (1992-2000) and Columbia University (2000-2011), and transitioned to UCLA in 2011.
In 2005, with the completion of the Cardiac Allograft Rejection Gene-expression Observational (CARGO) study (Deng 2005), there was a need to further explore information about thousands of genes collected in many samples that we decided to embark on. The CARGO study was a an important milestone that ignited new research, controversy and hopes to continue improving the armamentarium we have to care for our heart failure patients to improve their outcomes.
The evolution of mechanical circulatory support (MCS) therapy, and the improvement of the knowledge obtained initially within the ISHLT MCS database (Deng 2005) and later on with the US-INTERMACS Registry leading to the recognition of specific subgroups of patients whom, despite applying the most current methodologies, continued to do poorly after MCSD and based on years of inflammation research and understanding leukocyte-endothelial cells interactions, we embarked on the MultiOrgan Dysfunction-Expression profiling (MOD-E) project (Sinha 2010).
The Advanced Heart Failure Research Laboratory has its roots at Stanford University (1992-1993), evolved at Muenster University (1992-2000) and Columbia University (2000-2011), and transitioned to UCLA in 2011.
In 2005, with the completion of the Cardiac Allograft Rejection Gene-expression Observational (CARGO) study (Deng 2005), there was a need to further explore information about thousands of genes collected in many samples that we decided to embark on. The CARGO study was a an important milestone that ignited new research, controversy and hopes to continue improving the armamentarium we have to care for our heart failure patients to improve their outcomes.
The evolution of mechanical circulatory support (MCS) therapy, and the improvement of the knowledge obtained initially within the ISHLT MCS database (Deng 2005) and later on with the US-INTERMACS Registry leading to the recognition of specific subgroups of patients whom, despite applying the most current methodologies, continued to do poorly after MCSD and based on years of inflammation research and understanding leukocyte-endothelial cells interactions, we embarked on the MultiOrgan Dysfunction-Expression profiling (MOD-E) project (Sinha 2010).