Many studies have shown that strain measurements are becoming viable for diagnostic and clinical purposes. Strain has shown potential in serving as early indicator for a host of cardiac diseases such coronary disease, hypertension, etc. Therefore, it is crucial to develop techniques to accurately determine strain. There are many different methods to measure cardiac regional mechanics using a variety of techniques such as Doppler echocardiographic imaging as well harmonic phase algorithm (HARP). These methods are popular, as they have produced accurate systolic strains. However, both methods have their limitations. Previous studies have combined HARP with finite element modeling to compute 3D circumferential, radial and longitudinal strains in mice, however they limited their calculations to the left ventricle. Here, we use combine MRI, DT-MRI, and HARP to measure the same distributions, but in addition, we measure fiber, sheet- normal and cross-fiber strains in both the left and right ventricle. In order to examine this structure-function relationship, we will determine regional function in the left and right ventricle using a structure-dependent computational model of cardiac mechanics. Using normotensive and hypertensive rat hearts models, we will quantify the time course of regional strain throughout the left and right ventricle. These measures, along with ECG and blood pressures, will be used as inputs to a finite element model of the contracting ventricles. The goal of these studies will be to determine if these measures are sufficient to produce accurate strain fields in rat hearts

¹⁸F-clofarabine, a nucleotide purine analog, is a substrate for deoxycytidine kinase (dCK), a key enzyme in the deoxyribonucleoside salvage pathway. ¹⁸F-clofarabine might be used to measure dCK expression and thus serve as a predictive biomarker for tumor responses to dCK-dependent prodrugs or small-molecule dCK inhibitors, respectively. As a prerequisite for clinical translation, we determined the human whole-body and organ dosimetry of ¹⁸F-clofarabine. Methods: Five healthy volunteers were injected intravenously with 232.4 ± 1.5 MBq of ¹⁸F-clofarabine. Immediately after tracer injection, a dynamic scan of the entire chest was acquired for 30 min. This was followed by 3 static whole-body scans at 45, 90, and 135 min after tracer injection. Regions of interest were drawn around multiple organs on the CT scan and copied to the PET scans. Organ activity was determined and absorbed dose was estimated with OLINDA/EXM software. Results: The urinary bladder (critical organ), liver, kidney, and spleen exhibited the highest uptake. For an activity of 250 MBq, the absorbed doses in the bladder, liver, kidney, and spleen were 58.5, 6.6, 6.3, and 4.3 mGy, respectively. The average effective dose coefficient was 5.1 mSv. Conclusion: Our results hint that ¹⁸F-clofarabine can be used safely in humans to measure tissue dCK expression. Future studies will determine whether ¹⁸F-clofarabine may serve as a predictive biomarker for responses to dCK-dependent prodrugs or small-molecule dCK inhibitors.