Quantify the capacity of HUVECs to form capillary-like tubular networks on basement-membrane matrix and measure how pro-angiogenic (VEGF) and anti-angiogenic (suramin, bevacizumab) treatments modulate network metrics such as total tube length, branch points, and number of meshes.
Measure intracellular Ca2+ transient amplitude, rise time, decay tau, and beat rate in hiPSC-cardiomyocytes loaded with the fluorescent indicator Fluo-4 AM, to quantify how pharmacological modulators (isoproterenol, caffeine, nifedipine) alter excitation-contraction coupling and SR Ca2+ handling.
Quantify cardiomyocyte cross-sectional area in pressure-overload (transverse aortic constriction) versus sham mouse hearts using wheat-germ-agglutinin (WGA) membrane labeling, to objectively measure cellular hypertrophy underlying pathological cardiac remodeling.
Quantify drug-induced changes in field-potential duration, beat rate, and conduction velocity in syncytial hiPSC-cardiomyocyte monolayers on a microelectrode array to detect proarrhythmic liability (e.g., hERG-mediated repolarization delay and early afterdepolarizations).
Generate >80% pure, spontaneously contracting ventricular-like cardiomyocytes from human induced pluripotent stem cells using temporally controlled small-molecule Wnt/β-catenin modulation, suitable for downstream electrophysiology and disease modeling.